UTA Patho Final

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111 Terms

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Hyperplasia

Increased multiplication of cells

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Rheumatoid Arthritis VS. Osteoarthritis

RA occurs all over body, in younger peopleworse in the morning, requires a blood test

OA worse at night and occurs in older people, wear down of protective cartilage

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Opportunistic deseases seen in AIDS patients

Thrush, Pneumoctstis pnemonia (PCP), Cytomegalovirus (CMV), Kaposi Sarcoma (Causes lesions)

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What can cause bloody diarrhea?

Dysentery, IBS, Crohn's

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Lymohademopathy

enlarged lymph nodes bc of infection or cancer

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Hypersplenism

overactive spleen-WBC, RBC, platelets get eaten

S/S anemia, leukopenia, thrombocytopenia, pancytopenia

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Spleenomegaly

enlargment of the spleen

causes: increased hemolysis of RBC

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Chronic venous insufficiency (CVI)

ploppy veins and valves, poor venous return,

S/S edema, brown skin, breaks in skin that cant heal bc can't get though edema

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Polycythemia Vera

Blood cancer that causes an overproduction of RBC making blood thick and sludgy treated by donating blood

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Deep vein thrombosis (DVT)

Caused by virchow's triad

S/S swelling, redness, warm

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Virchow's Triad

Venous stasis- Hypercoaguability- vascular wall injury

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Pulmonary Embolism

S/S SOB bloody sputum, right heart backflow

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Arterial insufficiency

Plaque build up,hardening of walls

etiology: genetics, lack of exercise, diet, alcoholism, smoking

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Peripheral Arterial disease (PAD)

Narrowed blood vessels cause lack of blood flow

S/S Pain, Paresthesia (prickly burning), Pallor (unhealthily pale)

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Terratogenic influences on pregnant woman

drugs, alcohol

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Alternative name for Down syndrome

Trisomy 21

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3 single gene disorders

autosomal recessive, autosomal dominant,

sex-linked

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Carcinoma

malignant epithelium (Skin cancer)

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Dysplasia

abnormal growth of cells, tissues, bone, or an organ

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McCardle's disease

a glycogen storage disease

S/S Muscle pain, weakness,cramps, exercise intolerance

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Beriberi disease

Lack of thiamine (B1)causing problems with Memory and parasthesia

etiology: alcoholism, poor diet

S/S SOB, swollen legs, pain

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Sickle cell anemia

Autosomal recessive disease

mutates RBC C shaped

S/S SOB, fatigue, ischemia esp, in joints

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Metaplasia

Reversible replacement of one differentiated cell type with another

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Kwashiorkor

protein malnutrition from diet

S/S swollen belly in children, frequent infection

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Sarcoma

malignant connective tissue (bones, soft tissue)

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Hypertrophy

abnormal enlargement of a body part or organ

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Wernicke sydrome

B1 thiamine deficiency due to alcoholism

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Venous stasis from congestion causes

increased hydrostatic pressure leading to:

edema

varicose veins(twisted veins)

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S/S of Edema

dry tight skin, brownish discoloration, venous ulcers

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CVI factors

Age, inherited predisposition, obesity, pregnancy, poor muscle tone from immobility

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Thrombophlebitis

inflammation and swelling of vein from clot(DVT)

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Virchow's Triad is present in people who

Sit for long periods

have casts

pregnant

obese

on diuretic medication

have preexisiting problems such as circulation, clotting probs

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Pulmonary Embolism S/S

Can occur due to DVT

chest pain

SOB

hemoptysis

shock

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Treating venous probs (DVT,PE)

mobility

hydration

elevate legs

blood thinners

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Systolic pressure

Diastolic pressure

-Pressure on arteries when heart is contracting and ejecting blood

-Pressure when heart is resting

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Good perfusion

110/60, pulses can be felt, palpable arteries, nail blanching, normal organ function

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Arteriosclerosis

chronic disease of arterial system

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Arteriosclerosis etiology

HTN, smoking,diabetes, infectin, high cholesteral, microscopic damage,

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Atherosclerosis

fat deposits in wall causing inflammation and coagulatory response

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Patho of aterio disease

Ischemic pain(increase with exertion)

pale,cool skin

delayed healing

altered level of consciousness

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Peripheral arterial disease (PAD)

commonly applies to legs but any arterial disease outside of the heart

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Venous thrombi

Block flow toward heart

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Etiology for Hypertension

Atherosclerosis

Overactive sympathetic nervous system

Overactive RAAS

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Overactive sympathetic system patho

Over-relase of epinephrine by cariac symp nerve fibers---Over stimulates beta receptors of heart muscle which INCREASES HR and contractility

resulting in GREATER CARDIAC OUTPUT

larger volume of blood in peripheral arteries lead to sustained increased BP

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Damage done by Hypertension

Neuological (loss of funtion in brain due to ischemia)

Renal (spilling of blood or protein into urine eventually leading to renal failure)

Cardiovascular (increased workload stiffens arteries leading to high BP)

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hematuria

blood in urine due to high pressures

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proteinuria

protein found in urine due to high pressure

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Aneurysms

dilated or out-pouching of arterial vessel wall from

weakened arterial walls

injury to the intima allowing blood to seep into arterial muscles and tissues

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Aneurysm S/S

if leaks or ruptures in brain

weakness on one side of the body

change in level of consciousness

headache

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How to prevent HTN/ arterial disease

manage stress, smoking, alcohol

Lower LDL and HDL

exercise

increase good fat

Beta-blockers to help sympathetic overactivity

ACE inhibitor to help RAAS overactivity

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RUQ contains

liver&gall bladder, part of pancreas, part of transverse colon

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LUQ contains

part of stomach, spleen, part of transverse colon

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RLQ contains

cecum, appendix, part of ascending colon

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LLQ contains

Part of descending colon, sigmoid colon

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Umbilical region contains

lower duodenum, jejunum, ileum

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epigastric area contains

pyloric area of stomach, duodenum, art of pancreas

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Gastroesophageal reflux disorder (GERD)

reflux of hydrochloric acid and pepsin from stomach into esophagus--due to relaxation of lower esophageal sphinctor

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Barrett's esophagus

Tissue in esophagus becomes dysplastic (precancerous) due to GERD

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Hiatal heria

stomach herniates through the diaphragm causing GERD, dysphagia (difficulty swallowing)

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Gastritis

inflammation of gastric tissue can cause erosion

S/S pain, burning, bleeding

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acute gastritis

results from overuse of NSAIDS (suppress protective prostaglandins) or ETOH (alcohol)

heals once offending agent is removed

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Chronic gastritis (atrophic gastritis)

Autoimmune etiology

occurs in elderly

DEVELOP pernicious anemia

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Peptic Ulcer disease (PUD)

inflammation of stomach and proximal duodenum mucosal lining allowing acid to ulcerate underlying tissue causing ULCERS

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Causes of PUD

ASA(aspirin)

NSAID ALl DECREASE PROSTAGLANDINS

Chronic steroids

Heavy alcohol use

chronic disease such as liver,CKD,diabetes

Psychological stress

H.Pylori

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Heliobacter Pylori

bacteria ingested that burrows past mucous lining and attatches to epithelial cells

S/Spain after eating

GI bleeding

Treated by antiacids and eradicated by antibiotics

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Colorectal cancer

S/S blood in stool

changes in bowel habits

TX if confined to polyp- polypectomy

if widespread removal of part of colon leading to colostomy

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Inflammatory bowl disease

inflamm of lining and walls of intestines

Crohn's disease

ulcerative colitis

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Fistula

abnormal channels or connection of organs

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Crohn's disease (small intestines)

Transmural involvement (all layers of bowl are inflamed )

Patchy pattern

S/S malabsorption, bloody diarrhea, abdominal cramps, weight loss

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Ulcerative colitis (large intestine colon disease)

Ulcers begin in rectum and progress into entire colon

confluent segments of inflamed tissue

do not extrend beyond submucosa

S/S main difference-- dehydration

not at risk for malnutrition

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Patho of an intestinal obstruction

Obstruction- buildup of fluid and gas proxima; to obst.- adbominal distention

S/S colicky abdominal pain

constipation

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causes of bowl obstruction

adhesions (scaring)

hernia

tumor

intussusception ( telescope portion of bowel cutting blood)

volvulus (tortion)

paralytic ileus (loss of motion)

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Paralytic illus caused by

post anesthesia, abdominal surgery. electrolyte imbalance, spinal trauma

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Diverticulum/ diverticulosis

herniation of mucosa from muscle layer of intestine protruding out

No symtoms

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Diverticulitis

inflammation and pain of diverticula

S/S LLQ pain, feve, leukocytosis

abscess formation, rupture

TX increase fiber, avoid seeds/nuts, anitbiotics'

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UGI

bleeding from upper GI

esophagus, stomach, deodenum

S/S hematemesis( vomit)

frank bleeding (brown color, partially digested)

Occult bleeding (trace amount from chronic bleeding)

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LGI

bleeding from lower GI

jejunum, ileum. colon

IBD, diverticulitis, neoplasms

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Hematochezia

blood in the stool

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Jaundice

alteration in bilirubin cycle where it gets deposited in various places manifesting as yellow-green skin

Prehepatic, hepatic, posthepatic

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Prehepatic Jaundice

increased unconjugated bilirubin which occurs when hemolysis rate is faster then livers ability to process bilirubin

hemolytic anemia( decreased RBC bc of destruction) or erythroblastosis fetalis

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Posthepatic jaundice (obstructive)

Increased conjugated bilirubin(direct bilirubin) problem with bilirubin making into intestines due to obstruction or inflammation (ex:tumor)

backs up and leaks from liver cells into circulation

Makes stool grey

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Hepatic jaundice

increased unconj bili from cirrhosis or hepatitis so liver cannot conjuate and conjuate bili is low

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Prehepatic Blood test

bili serum- high

Indirect (unconjugated bili)- high

direct bili-normal

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posthepatic blood test

bili serum- high

Indirect (unconjugated bili)- normal

direct bili- high

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hepatic blood test

bili serum-high or norm

Indirect (unconjugated bili)- high

direct bili-low

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Cholecystitis

inflammation of gall bladder caused by stones

from cholesterol increase

dehydration

S/S pain in RUQ

biliary colic (spasms of GB and bile ducts) worse after high fat meal

nausea/vomiting

posthepatic jaundice

risk factors female, fat, forty, fertile, fair

starvation

obesity

Labs: high direct bili

leukocytosis

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Acute Pancreatitis

escape of pancreatic enzyme into pancreas and surrounding causing AUTODIGESTION

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Pancreatic cancer

S/S pain, jaundice, weightloss

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Hepatits

inflammation of the liver from autoimmune probs, microbs, idiopathic

S/S aching, fatigue, malaise, Nausea, vomiting, jaundice

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viral hepatitis

HAV,

fever, malaise, jaundice

mild transmitted externally (oysters)

HBV, HCV,

transmitted parenterally (outside gut)

IV abuse, recieving blood, sexually

insidious

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Cirrhosis

end stage irreversible liver disease

MAinly from alcohol abuse

toxic reaction to drugs

viral hepatitis

primary bili cirrhosis

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cirrhosis patho

Diminished hepatocyte function leading to

-nutritional problems (glyconeogenesis, glycogenolysis)

-protein depletion probs (low protein lead to ascites(B-T abdomen) and less clotting factor

-metabolism probs incuding ammonia, drugs, hormones

-Portal HTN

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Hempatic encephalopathy

result of cirrhosis- cannot metabloize ammonia leading to toxic levels in CNS leading to brain inflammation

S/S

lack of mental awareness, confusion, coma

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Asterixis

liver flap-- flapping tremor of hands as result of cirrhosis

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Ascites

increased back pressure into portal veins-increased hydrostatic pressure- fluid into abdominal cavity

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Splenomegaly

shunting of blood into splenic vein enlarges spleen

develops hypersplenism (breakdown of RBC, WBC, thrombocytes

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Varices

enlarged, thin walled veins

worse in esophagus bc it can easily rupture and bleed to death

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Tests for Cirrhosis

check bilirubin levels

elevated serum liver enzymes check

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Treatment for liver disease

enhance nutrition, no alcohol,

give diuretics to move T-B

IV albumin

control ammoina

protect against infection, trauma,

liver transplant

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WHen HR is faster than normal

SNS fight or flight (epinephrine secreted binds to beta receptors)

Hyperkalemia causing hyopolarization

SA, AV node glitches