FINAL PATHO

I want to cry

gastritis def

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acute? what is it triggered by?

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chronic, what does it lead to?

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what can cause chronic?

inflammation of the stomach lining

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triggered by ingestion of toxins or as consequence of viral, bacterial, autoimmune illnesses

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may lead to atrophy of gastric mucosa, resulting in decreased hydrochloric acid and intrinsic factor production

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H. pylori, achlorhdia (reduced hydrochloric acid production), PUD, atrophic gastritis, gastric carcinoma, lymphoma

Peptic ulcer disease (PUD) def

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major causes?

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upper GI organs?

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what do NSAIDs do?

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management

disorder of upper GI tract caused by action of pepsin and hydrochloric acid

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H. pylori and NSAIDS

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mouth, esophagus, stomach, duodenum

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they inhibit prostaglandins which are used as a protective mucosal barrier. when prostaglandins are taken away, stomach acid erodes tissue which increases the risk for ulcers, inflammation, iron deficiency anemia due to chronic blood loss

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minimize acid secretion (proton pump inhibitors), eradicating H. pylori, and stop smoking

common risk factors for PUD

stress
H. pylori
alcohol
smoking
family history

duodenal ulcers factors and info, cause

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stress ulcers factors and info

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gastric ulcers factors and info, cause

most common
well nourished
pain 2-3 hours after meals
food may decrease pain
cause: excessive acid secretion mediated by inc vagal activity

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physiological stress, shock
Cushing's Ulcer-brain injury
curling's ulcer - extensive burns

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weight loss
HCL-normal or hyposecretion
pain 1/2 - 1 hr after meals
vomiting, eating may increase pain
cause: breakdown of protective mucous layer that normally prevents diffusion of acids into gastric epithelia

pepsin, a proteolytic enzyme found in the GI tract, is converted from its precursor form, pepsinogen, in the presence of:

HCL (acid) secretions in the stomach

Helicobacter pylori infection: common precursos for?

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risk factor

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what does it synthesize?

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what does ammonia do?

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treatment:

precursor of gastritis and peptic ulcers

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gastric carcinoma

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synthesizes urease, which produces ammonia that damages the gastric mucosa

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neutralizes acid pH, which allows organism to live in stomach

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omeprazole, amoxicillin, clarithromycin

ulcerative colitis

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sx

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term for rectal bleeding

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management

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increased risk for what?

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inflammatory disease of mucosa of rectum and colon (mucosal layer of bowel), disordered immunity and mucosal inflammation

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abdominal pain, cramping, diarrhea rectal bleeding, weight loss

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hematochezia

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systemic corticosteroids, anti-TNF (tumor necrosis factor) agents, surgical colectomy, antibiotics, sulfasalazine

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risk for colon cancer for those who've had it for more than 7-10 years

Crohn's disease def

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also called

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commonly affects what parts?

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what are common?

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treatment

* inflammation of GI tract that extends through all layers of intestinal wall

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* regional enteritis or granulomatous colitis

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* proximal part of colon and terminal ileum

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* multiple portions of colon with intervening normal areas left between affected regions

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* colostomy and ileostomy, decrease inflammation with drug therapy

Crohn's disease factors

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sx

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later s/sx

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complications

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management

familial tendencies, peaks ages 15-40, not sure about autoimmune factors

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nausea and vomiting, abdominal pain/distention, tenderness in RLQ, severe diarrhea, low grade fever, bloody stools, weight loss, severe malabsorption (bc of diseased bowel)

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dehydration, electrolyte imbalance, anemia

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intra-abdominal abscesses, intestinal fistulas, peritonitis, development of fistulas

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reduce inflammation (w/drug therapy), and maintain remission

fistula

abnormal connection between an organ, vessel, or intestine and another organ, vessel, intestine, skin

when do UC and Crohn's usually develop?

young adulthood

dysphagia

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problems (3)

difficulty swallowing

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delivery of bolus into esophagus bc of neuromuscular incoordination

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transport of bolus (stuck) down body of esophagus bc of altered esophageal peristaltic activity

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bolus entry into stomach bc of LES dysfunction or obstructing lesions

esophageal pain

heartburn
midsternal somatic pain, mimics angina pectoris from esophageal distention and obstruction

abdominal pain 3 times

visceral (diffuse, poorly localized)
somatic (sharp, well localized)
referred (at a distance from source but in same dermatome)

hematemesis

blood in vomitus

constipation

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treat

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what happens if you don't solve

small, infrequent, or difficult bowel movements
less than 3x a week

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inc fluid intake, inc fiber, laxative (especially if on opioid), early ambulation

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bowel obstruction and perforation

diarrhea

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osmotic

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secretory

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exudative

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melena

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hematochezia

increased frequency and fluidity of bowel movements

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inc amounts of poorly absorbed solutes in intestine

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caused by toxins that stimulate intestinal fluid secretion, impair absorption

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mucus, blood, protein, inflammatory processes

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malodorous, liquid, black tarry stool

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feces with bright right blood (UC or hemorrhoid)

bowel obstruction

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higher obstruction the what?

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bowel sounds with constipation

mechanical blockage or paralytic ileus

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quicker the symptoms

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increased to silent
high pitched at first then go silent

gastroesophageal reflux disease (GERD) def

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symptomatic?

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esophagitis (present as)

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complications

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pulmonary sx

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what can chronic GERD cause

backflow of gastric contents into esophagus through LES (lower esophageal sphincter)

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may or may not be

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esophageal inflammation caused by highly acidic refluxed material, heartburn, chest pain, dysphagia

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esophageal strictures

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reflux esophagitis (cough, asthma, laryngitis)

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Barrett esophagus (normal squamous epithelium of distal esophagus is replaced by columnar tissue)

hiatal hernia

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sx

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2 types

defect in diaphragm that allows portion of stomach to pass through diaphragmatic opening into thorax

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heartburn, chest pain, dysphagia (esophageal reflux accompanies)

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sliding: portion of stomach slips up into thorax, gastroesophageal junction above diaphragmatic opening

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paraesophageal: part of greater curvature of stomach rolls through diaphragmatic defect

mallory-weiss syndrome

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what is it caused by?

bleeding caused by a longitudinal tear in mucosa or submucosa of cardia or lower portion of esophagus

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forceful or prolonged vomiting during which esophageal sphincter fails tor elax

esophageal varices

abnormal veins in lower part of esophagus, develop when blood flow to liver is blocked

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rupture of esophageal varices is a serious complication of cirrhosis-induced portal hypertension and carries a high mortality rate

heartburn is mostly likely the consequence of what?

backflow of gastric contents into esophagus

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stim of esophageal sensory nerve endings

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defect in diaphragm

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esophageal spasm

Hepatocellular failure

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jaundice

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sx

impaired processing of endogenous steroid hormones and byproducts of protein metabolism and decreased clearance of exogenous drugs and toxins

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green-yellow staining of tissues by bilirubin (consequence of impaired bilirubin metabolism)

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muscle wasting, ascites, excessive bleeding (coagulopathy), blood protein and vitamin deficiencies (hypoalbuminemia, A, D, E, K), glucose imbalance, impaired hormone production

prehepatic

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hepatic

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posthepatic

transfusion reactions, sickle cell anemia, thalassemia, autoimmune disease

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hepatitis, cancer, cirrhosis, congenital disorders, drugs

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gallstones, inflammation, scar tissue, tumors block flow of bile into intestines

portal hypertension

condition resulting from impaired blood flow through liver as a result of increased resistance from fibrosis and degeneration of liver tissue

gastroesophageal varices

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sx

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treatment

result from portal hypertension
result of cirrhosis caused by chronic alcoholism or viral hepatitis, or chronic infection with Schistosoma species of liver fluke (parasitic ova)

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hematemesis, melena, red rectal bleeding, anemia, shock

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fluid resuscitation, correct coagulopathy, stop bleeding, lower portal pressure, EGD (emergency esophagastroduodenoscopy)

hepatic encephalopathy

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cause

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sx

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problem increased by

complex neuropsychiatric syndrome, abnormal protein metabolism

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increase in blood ammonia

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mild confusion that progresses to stupor and coma
impaired thinking/judgement
neuromuscular disturbances
asterixis (liver flap)
hyperreflexia

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inc protein, infection, hypovolemia, hypokalemia, GI bleeding

cerebral edema

results in?

serious complications in patients w/ grade 3 or 4 hepatic encephalopathy

inc in intracranial pressure

ascites

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causes

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retention?

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treatment

pathologic accumulation of fluid in peritoneal cavity

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portal hypertension and hypoalbuminemia

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sodium and water, low serum albumin secondary to decreased hepatic synthesis

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sodium retention, diuretics, intermittent paracentesis, surgical shunting

cirrhosis

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sx

diffuse hepatic fibrosis surrounding nodules of liver tissue and results in permanent alteration in hepatic blood flow and liver function

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jaundice
esophageal varices
ascites
hepatomegaly, splenomegaly
hemorrhoids
edema, peripheral neuropathy
sexual characteristic changes (gynecomastia, hirsutism)
palmar erythema
superficial veins visible on ab wall
anemia, leukopenia, thrombocytopenia, coagulation disorders
spider angiomas (face, neck, shoulders)
changes in mental responsiveness and memory
impaired production of clotting factors

leukopenia

thrombocytopenia

thrombocytosis

low WBC count

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low platelet level

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too many platelets

conjugation

process of converting bilirubin from freely lipid-soluble form to form that is tightly bound to plasma protein albumin

what is jaundice due to?

increased quantities of unconjugated bilirubin

the development of esophageal varices in cirrhosis is related to

hepatic fibrosis caused increased resistance to portal circulation

acute viral hepatitis

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what is needed to determine type?

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type A

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type B

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type C

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type D

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type E

inflammation of liver parenchyma, caused by infection

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serologic testing

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RNA virus spread enterically (contained food/h2o), yes vaccine

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partially double-strand DNA, body fluids, yes vaccine

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single-stranded RNA to Flavivirdae family, circulation, no vaccine

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incomplete viral organism that needs HBV for replication (no D w/out B), no vaccine, blood transmission

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RNA virus spread via fecal-oral route (bowel), no vaccine

hepatitis sx

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treatment

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diagnosis

RUQ discomfort, anorexia, weight loss
fever, chills, jaundice, dark urine, history of potential exposure

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rest, activity as tolerated, nutrition, hydration

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presence of specific antibody/antigen in serum

patho of shock

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what is common denominator in all forms

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what does inadequate oxygen availability impair?

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what does oxygen deprivation cascade result in?

imbalance between oxygen supply and oxygen requirements at cellular level

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impaired tissue oxygenation

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aerobic metabolism of glucose, fatty acids, amino acids, causes cells to rely on glycolysis to produce cellular ATP

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formation of oxygen free radicals
induction of inflammatory cytokines

early signs of shock

normal or a little decreased MAP
normal or inc heart rate
normal to decreased urine output
pale and cool skin
anxious
inc rate and inc depth of breathing

late signs of shock

hypotension, really low MAP
tachycardia
very low urine output 0.5 ml/kg/hr
cool, moist, mottled skin
dec LOC
inc rate, shallow breaths

compensatory stage of shock

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manifestations of SNS activation

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what is kept even though cardiac output dec?

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sx

homeostatic mechanisms maintain adequate tissue perfusion despite a reduction in cardiac output

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tachycardia, inc myocardial stim, bronchodilation, vasoconstriction, cool clammy skin, dilated pupils, dec urine output

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blood pressure

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MAP dec, inc renin and ADH and heart rate
dec pulse pressure and pH
restlessness, apprehensive

progressive stage of shock

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shift of cells to what results in what

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lack of what production leads to what

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generation of what?

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release of what?

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activation of what?

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all lead to what?

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sx

compensatory mechanisms fail, hypotension and progressive tissue hypoxia result

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anaerobic metabolism, lactate production and metabolic acidosis

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lack of ATP production = cellular swelling, dysfunction, death

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oxygen free radicals

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inflammatory cytokines

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clotting cascade

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cellular and organ dysfunction

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MAP dec even more, tissue/organ hypoxia
oliguria, weak rapid pulse, dec pH, sensory neural changes

refractory stage of shock

sx

organ failure
unresponsive to therapeutic interventions

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excessive cell/organ damage
multi system organ failure
dec pH

cardiogenic shock

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what occurs

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sx

severe ventricular dysfunction associated with MI, cardiomyopathy, ventricular rupture, congenital heart defects

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dec cardiac output, elevated L ventricular end-diastolic pressure (preload), pulm edema

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inc heart rate, vasoconstriction, narrow pulse pressure

obstructive shock

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causes

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sx

heart is prevented from pumping bc of a mechanical obstruction to blood flow

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pulmonary emoblism, cardiac tamponade, tension pneumothorax

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R HF sx

hypovolemic shock

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sx

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treatment

inadequate circulating blood volume precipitated by hemorrhage, burns, dehydration, leakage of fluid into interstitial spaces

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elevated heart rate, vasoconstriction, inc myocardial contractility

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fluid replacement (isotonic) and control of volume loss

distributive shock

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anaphylactic shock (sx)

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neurogenic shock

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septic shock

excessive vasodilation and peripheral pooling of blood

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excessive mast cell degranulation in response to antigen
severe hypotension, urticaria, bronchoconstriction, stridor, wheezing, itching

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results from loss of sympathetic activation of arteriolar smooth muscle

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results from severe systemic inflammatory response to infection

complications of shock


acute respiratory distress syndrome

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disseminated intravascular coagulation

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acute renal failure

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inflammation triggered by?

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what does excessive immune system responses lead to

reduced cellular oxygen consumption, may affect all organs
respiratory failure

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abnormal clot formation in microvasculature throughout body

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kidney failure

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hypoxic injury to cells by antigen or by endotoxin

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leaking capillaries, damage from proteolytic enzymes, systemic activation of clotting, complement, kinin systems

multiple organ dysfunction sydrome

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primary

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secondary

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what is mortality rate affected by?

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2+ organs failed

5+ organs failed

initiated by immune mechanisms that are overactive and destructive, ongoing inflammation leads to tissue destruction and organ dysfunction

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trauma sepsis

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septic shock most common

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systemic inflammatory response system # of organs affected

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54% 100%

hematocrit male

female

total leukocyte count

40-50%

27-47%

5,000-10,000/uL

sodium

potassium

total calcium

ionized calcium

magnesium

chloride

phosphate

135-145 mEq/L

3.5-5.0 mEq/L

8.5-10.5 mg/dL

4.5-5.6 mg/dL

1.8-3.0 mEq/L

95-105 mEq/L

2.4-4.5 mg/dL

hydropic swelling

intracellular accumulations

cellular swelling attributable to accumulation of water
Na+ and H2O accumulation

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excess accumulations of substances in cells (fat)
abnormal substances accumulate produced by cell bc of faulty metabolism

atrophy

hypertrophy

hyperplasia

metaplasia

dysplasia

cell shrinkage bc of chronic ischemia or dec funct demand

cell size increases bc of physiologic and patho demands

cell number increases bc of chronic irritation/cell injury

a normal cell is replaced by another normal cell bc of adaptation to a persistent injury (new cell type better for the situation)

abnormal development or growth of cells, tissues, organs, maladaptive (adaptive effort gone astray)

necrosis

irreversible cell injury
consequence of ischemia or toxic injury when it's prolonged
cell rupture, contents spilling into ECF, inflammation
breakdown of plasma membrane, organelles, and nucleus
initiates an inflammatory response

coagulative necrosis

liquefactive necrosis

caseous necrosis

fat necrosis

cell proteins altered from gelatinous to firm/opaque, anywhere but brain bc of ischemia

cells digested by own degradative enzymes so tissue becomes soft (lack of O2)

cells disintegrate but aren't completely digested (soft granular clump)

fatty tissue is broken down into fatty acids in the presence of infection or certain enzymes
opaque, soap-like lesions

apoptosis

what is it triggered by

programmed cell death
process is tidy and doesn't elicit inflammation
phagocytosis of apoptotic cell and fragments

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environmental or extrinsic signals
extracellular signals
internal pathways

ischemia

tissue hypoxia

Lack of blood supply

most common cause of cell injury in clinical medicine

cell death may be slow to develop

most cellular damage occurs after the blood supply to the tissues has been restored

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results from poor oxygenation of the blood (hypoxemia)

most often caused by ischemia

ischemia-reperfusion injury

injury to tissue that occurs after blood flow is restored
following an ischemic episode results in increased free radical production and leads to further tissue damage due to excessive intracellular calcium, subsequent inflammation

etiology of cellular injury

ischemic and hypoxic, nutritional, infections and immunologic injury, chemical injury
decrease in ATP, failure of Na/K pump, hydropic swelling, use of anerobic metabolism

somatic death

whole body death

inflammatory response purposes

neutralize and destroy invading and harmful agents
limit the spread of harmful agents to other tissue
prepare any damaged tissue for repair

5 cardinal signs of inflammation

redness (rubor)
swelling (tumor)
heat (calor)
pain (dolor)
loss of function (functio laesa)

inflammation

a localized response to an injury or to the destruction of tissues
increased vascular permeability
emigration of leukocytes
phagocytosis
chronic inflammation

which leukocyte comes first in inflammation?

eosinophils

basophils & mast cells

monocytes and macrophages

what type of immunity are these?

what granules release chemicals?

which cells are phagocytic

neutrophils 60-80%

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allergic reactions, parasite infection

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contain histamine, mediate type I allergic reactions, initiate inflammation

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come from bone marrow stem cells (myeloid)
monocytes are immature macrophages

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innate immunity (rapid response)

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basophils & mast cells

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neutrophils, macrophages, monocytes

T cell

Natural killer T cell

CD4

CD 8

form in the thymus and other lymphatic tissue and attack cancer cells, viruses, and foreign substances
cell-mediated immunity
branch off into CD4+ and CD8+ cells

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A type of white blood cell that can kill tumor cells and virus-infected cells; an important component of innate immunity.

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T helper cells interact with the antigens that are on the surface of the dendritic/macrophages/ and B cells.

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Cytotoxic t cells recognize the antigen on the cells and kills it.

B lymphocytes

what kind of immunity?

form in the bone marrow and release antibodies that fight bacterial infections
antibody-mediated immunity

adaptive immunity (slow response)

healing, fibroblasts

healing, endothelial cells

healing, myofibroblasts

synthesize connective tissue and can move around

regenerate and stimulated by angiogenic substances to form new capillaries

develop at wound edges and induce wound contraction

systemic manifestations of inflammation

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what are these responses attributable to?

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Interleukin

fever, neutrophilia, lethargy, muscle catabolism, increased acute phase proteins (C-reactive protein), increased erythrocyte sedimentation rate

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interleukin (IL)-1, IL-6 and tissue necrosis factor-alpaha released from macrophages and inflamed tissues

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produced by macrophages & lymphocytes; response to a pathogen or stimulation by other products of inflammation

Acute inflammation

Chronic inflammation

good inflammation
serious threat triggers it (cut, bruise, infection...)
body releases inflammatory compounds
job gets done, anti-inflammatory compounds released, body ok

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bad inflammation
non-serious event triggers (eating food, acne bacteria)
body releases inflammatory compounds
body doesn't release anti-inflammatory compounds and keeps sending an inflammatory response

describe the steps that go into inflammation in order.

1. phagocytes go to an inflamed area, gather at the side of it, and PUSH into that area
2. neutrophils and macrophages travel to the inflamed areas by chemokines, selectins, and integrins that are located on the surface of endothelial and leukocyte cells
3. neutrophils swarm in huge and begin phagocytosis
4. neutrophils and macrophages create proteolytic enzymes and oxidizing agents to destroy and digest the antigen causing the inflammation

immunity

passive

active

what does the development of active immunity require?

what happens on second exposure to antigen?

state of resistance against infection from a particular pathogen

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involves transfer of plasma (sera) containing performed antibodies against a specific antigen form a protected or immunized person to an unprotected or non-immunized person

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confers a protected state attributable to the body's immune response as a result of active infection or inflammation

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the maturation and maintenance of memory B cells

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antibody response is greater and more rapid

naturally acquired immunity active

passive

antigens enter the body naturally, body induces antibodies and specialized lymphocytes

antibodies pass from mother to fetus via placenta or to infant via the mother's milk

artificially acquired active

passive

antigens introduced in vaccines, body produces antibodies and specialized lymphocytes

performed antibodies in immune serum are introduced by injection

hallmark of HIV

what are CD4+ cells necessary for?

decrease in CD4+ or T helper cells
defective cell-mediated immunity

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appropriate immune responsiveness
cells that mediate between antigen-presenting cells and other immune cells

HIV transmission

sexually (semen, vaginal secretions)
parenteral (blood, blood products, blood-contaminated needles or syringes)
perinatal (in utero, delivery, breast milk)

what CD4+ level count is a diagnosis of AIDS?

what is the key element in HIV infection?

less than 200

high level of virion production and the high level of CD4+ cell death

screening for HIV

enzyme immunoassay (EIA) at 3 weeks, 6 weeks, 3 months after exposure
rapid HIV antibody testing-tests for antigens, not antibodies, if positive
need follow-up with EIA and/or antibody/antigen test

seroconversion

window period

development of HIV specific antibodies

may be 2 months between infection and detection of antibodies (HIV positive)

AIDS diagnosis

presence of CD4+ cell count of less than 200
opportunistic infection (fungal, viral, bacterial, protozoal)
cancer (invasive cervical, kaposi's sarcoma, lymphoma)
wasting syndrome
AIDS dementia complex

early chronic infection HIV (HIV-AIDS development?

intermediate chronic infection

late chronic infection

11 years
sx: fatigue, headache, lymphadenopathy, low grade fever
normal CD4+ T-cell count, increased infections

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CD4+ cell count @ 200-500
increased viral load
increased infections, sx more severe

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diagnosis of AIDS

treatment for HIV

goals

antiretroviral therapy (ART) begins with confirmation of HIV

decrease viral load, maintain or increase CD4 count
delay onset of HIV related sx
prevent or delay any opportunistic infection

extracellular fluid volume deficit
cm

excess
cm

hemodilution
normal level
hemoconcentration

caused by removal of a sodium-containing fluid from the body
weight loss, tachycardia, dehydration

both vascular and interstitial areas have too much isotonic fluid
weight gain, distended neck veins (JVD), overhydration

12 gm Hgb, 27% Hct
12 gm Hgb, 36% Hct (Hct = 3xHgb)
12 gm Hgb, 47% Hct

hyponatremia
cause
sx

hypernatremia
sx

serum sodium concentration below the lower limit of normal
ECF excess (dilutional)
dec Na+ intake (depletional)
cause: ADH
seizures, confusion, lethargy, coma (cells swell, pressure inc)

serum sodium concentration above upper limit of normal
inc Na intake, dec excretion
dec H2O intake, inc excretion
no hormone
confusion, lethargy, coma (shriveled cell)

clinical dehydration

edema

combo of ECV deficit and hypernatremia

excess of fluid in the interstitial space

1. 0.9% NaCl

2. Lactated Ringers

3. D5W

4. D5 1/2 NS & 5. D5NS

1. used to expand volume, dilute medications, keep vein open (isotonic)

2. isotonic, used for fluid resuscitations

3. isotonic until inside the body, then metabolizes glucose and becomes hypotonic (don't give to infants or head injury patients bc it may cause cerebral edema), hydrate cells

4/5. used for Na and volume replacement
go slow, monitor BP, pulse rate, quality of lung sounds, serum Na and urine output (hypertonic)

hypertonic

isotonic

hypotonic

cells shrink, ECF more solute Na+

cell stays the same, equal ICF and ECF concentration

cell swells, ECF less solute so more water goes into the cell

hyperaldosteronism

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hypoaldosteronism

holding of Na+ and H2O, more Na+ into interstitial, pushes more K+ in the cell (leads to hypokalemia), not enough K+ in interstitial and vasculature

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not holding onto sodium, causes hyperkalemia, RAAS turns on to help

RAAS system

kidneys send decrease in BP and release renin from juxtoglomerular apparatus

renin converts angiotensinogen to angiotensin I

in lungs, angiotensin-converting enzyme (ACE) converts I to II

angiotensin II causes vasoconstriction, resulting in inc BP
also stimulates adrenal glands to release aldosterone

within kidneys, aldosterone promotes the reabsorption of sodium and water

circulating blood volume increases, raising BP

fluid distribution

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capillary hydrostatic pressure

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interstitial fluid hydrostatic pressure

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capillary colloid osmotic pressure

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interstitial fluid colloid osmotic pressure

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what can cause edema here?

between vascular and interstitial compartments, net result of filtration across permeable capillaries

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outward push of vascular fluid against the capillary walls

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outward push of interstitial fluid against the outside of the capillary walls

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inward-pulling forces of particles (proteins) in vascular fluid

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inward-pulling forces of particles (proteins) in interstitial fluid

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proteins --> interstitial = pulling fluid in vascular = edema

what does hypoventilation result in?
causes

what does hyperventilation result in?
causes

respiratory acidosis
drug overdose, pulmonary edema, chest trauma, neuromuscular disease, COPD, airway obstruction

respiratory alkalosis
initial stages of pulmonary emboli, hypoxia, fever, pregnancy, high altitudes, anxiety

metabolic acidosis

causes

sx

compensatory mechanism

pH below 7.40, abnormally low bicarb ion concentration
decreased ability of kidney to excrete acid or conserve base

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DKA, severe diarrhea, renal failure, shock, inc metabolic acid, dec bicarb

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headache, dec BP, hyperkalemia, muscle twitching, warm skin, nausea/vomiting/diarrhea, changes in LOC, kussmaul resp

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respiratory alkalosis (hyperventilation, decreases PaCO2, increases excretion of CO2 via Kussmaul respirations, kidneys excrete acid)

respiratory acidosis

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causes

\
sx

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compensatory mechanism

pH below 7.40 and abnormally high PaCO2
buildup for CO2 causes a buildup of carbonic acid (inc H+ ions, dec pH)

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hypoventilation
impaired gas exchange (asthma)
inadequate neuromuscular function (hypokalemic music function)
impairment of resp control in brainstem (opioid od)
COPD, pneumonia, atelectasis

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hypoventilation --> hypoxia
rapid, shallow resp, dec BP w/vasodilation, dyspnea, headache, hyperkalemia, dysrhythmias
drowsiness, dizziness, disorientation
muscle weakness, hyperreflexia

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metabolic alkalosis
excretion of H+ and retention of HCO3- by the kidneys
increases HCO3- concentration

metabolic alkalosis

causes

sx

compensatory mechanism

pH above 7.40 and abnormally high HCO3- concentration

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increase in base (bicarb)
decrease in acid (vomiting)
excessive GI suctioning
diuretics, excessive NaHCO3

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restlessness and lethargy
dysrhythmias (tachy)
compensatory hypoventilation
confusion (dec LOC, dizzy, irritable)
nausea, vomiting, diarrhea
tremors, muscle cramps, tingling of fingers/toes
hypokalemia

\
respiratory alkalosis
compensatory hypoventilation
increases PaCO2 levels, renal excretion of HCO3-
lungs kick in for metabolic issue, allows us to excrete bicarb

respiratory alkalosis

causes

sx

compensatory mechanism

pH above 7.40 and abnormally low PaCO2

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hyperventilation
happens bc of hysteria, anxiety, pain, fever
mechanical ventilation

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seizures, deep rapid breathing, hyperventilation, tachy, dec or normal BP, hypokalemia, numbness and tingling of extremities
lethargy and confusion
light headedness, nausea, vomiting

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metabolic acidosis
compensatory retention of H+
excretion of HCO3- by kidneys
decreases HCO3- concentration
rarely happens bc of aggressive treatment of hypoxemia

prediabetes

type I diabetes mellitus

type II diabetes

gestational diabetes
common complications

treatment

impaired glucose tolerance and impaired fasting glucose
intermediate stages between normal glucose metabolism and onset of diabetes
100-125 mg/dL

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characterized by destruction of beta cells of pancreas
can occur at any age but peaks at ages of 2, 4-6, 10-14

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resistance to action of insulin on peripheral tissues
affects 90-95% of individuals with diabetes in US

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disorder of glucose intolerance of variable severity with onset or first recognition during pregnancy
high infant birth weight and neonatal hypoglycemia
goes away after giving birth

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assessment of efficacy (monitor blood glucose and HbA1C levels)

type 1 s/sx

type 2 s/sx

polyuria, polyphagia, polydipsia
weight loss, fatigue, inc infection, rapid onset, insulin dependent, familial tendency

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polyuria, polyphagia, polydipsia
sedentary lifestyle
familial tendency
average age 50 yrs
inc Bp, dec energy
obese, recurrent infections
FBS > 126 mg/dL

acute hyperglycemia

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hypoglycemia causes, s/sx, treat

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nonketotic hyperglycemic hyperosmolar syndrome

commonly caused by alterations in nutrition, inactivty, inadequate use of antidiabetic medications, combo

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insufficient food, excess exercise, excess insulin
anxious, sweaty, hungry, confused, blurred vision, shaky, irritable, cool clammy skin, agitation, weakness, paresthesia (tingling)
coma, death unlikely
needs blood sugar increased

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more common in type II bc endogenous insulin suppresses ketone formation and prevents DKA

diabetic ketoacidosis (DKA)

history

sx

treatment

occurs primarily in type I as a result of increased lipolysis and conversion of ketone bodies, excessive ketones result in metabolic acidosis

lack of insulin, GI upset, febrile illness

fruity breath, kussmaul resp, dehydration, tachy, hypotension, acidosis, high blood sugar (>240), hyperkalemia, polyuria

needs hydration, insulin, electrolyte replacement

chronic hyperglycemia

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vascular complications

macrovascular

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microvascular

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retinopathy

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nephropathy

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neuropathy

has vascular complications, neuropathic (autonomic and sensory dysfunctions), skin complications, infection, pregnancy issues (infant mortality risk increases, anomalies)

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macro: damage to large blood vessels provide circulation to brain, heart, extremities, resulting from accelerated atherosclerosis

micro: small arterial vessels that supply retinae

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micro degenerative changes, thickening of cap membranes leads to obstruction and rupture, ischemia --> blindness

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protein breakdown, excessive osmotic diuresis and glomerular HTN, lead to glomerular hypoxia & sclerosis

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thick sclerotic blood vessels impaired supply to nerves
excessive glucose impairs myoinositol

nerves demyelinate due to impaired metabolism
can effect any part of nervous system but mostly lower extremities

thrombus

causes

what does arterial thrombosis result in?

what does venous thrombosis result in?

thrombophlebitis

stationary blood clot formed within a vessel or a chamber of heart

blood flow dramatically slows, turbulent flow, damage to intimal walls, drugs (oral contraceptives, tobacco, anesthetic)

ischemia

edema

inflammation with a clot in a vein