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Hyperplasia
Increased multiplication of cells
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
Opportunistic deseases seen in AIDS patients
Thrush, Pneumoctstis pnemonia (PCP), Cytomegalovirus (CMV), Kaposi Sarcoma (Causes lesions)
What can cause bloody diarrhea?
Dysentery, IBS, Crohn's
Lymohademopathy
enlarged lymph nodes bc of infection or cancer
Hypersplenism
overactive spleen-WBC, RBC, platelets get eaten
S/S anemia, leukopenia, thrombocytopenia, pancytopenia
Spleenomegaly
enlargment of the spleen
causes: increased hemolysis of RBC
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
Polycythemia Vera
Blood cancer that causes an overproduction of RBC making blood thick and sludgy treated by donating blood
Deep vein thrombosis (DVT)
Caused by virchow's triad
S/S swelling, redness, warm
Virchow's Triad
Venous stasis- Hypercoaguability- vascular wall injury
Pulmonary Embolism
S/S SOB bloody sputum, right heart backflow
Arterial insufficiency
Plaque build up,hardening of walls
etiology: genetics, lack of exercise, diet, alcoholism, smoking
Peripheral Arterial disease (PAD)
Narrowed blood vessels cause lack of blood flow
S/S Pain, Paresthesia (prickly burning), Pallor (unhealthily pale)
Terratogenic influences on pregnant woman
drugs, alcohol
Alternative name for Down syndrome
Trisomy 21
3 single gene disorders
autosomal recessive, autosomal dominant,
sex-linked
Carcinoma
malignant epithelium (Skin cancer)
Dysplasia
abnormal growth of cells, tissues, bone, or an organ
McCardle's disease
a glycogen storage disease
S/S Muscle pain, weakness,cramps, exercise intolerance
Beriberi disease
Lack of thiamine (B1)causing problems with Memory and parasthesia
etiology: alcoholism, poor diet
S/S SOB, swollen legs, pain
Sickle cell anemia
Autosomal recessive disease
mutates RBC C shaped
S/S SOB, fatigue, ischemia esp, in joints
Metaplasia
Reversible replacement of one differentiated cell type with another
Kwashiorkor
protein malnutrition from diet
S/S swollen belly in children, frequent infection
Sarcoma
malignant connective tissue (bones, soft tissue)
Hypertrophy
abnormal enlargement of a body part or organ
Wernicke sydrome
B1 thiamine deficiency due to alcoholism
Venous stasis from congestion causes
increased hydrostatic pressure leading to:
edema
varicose veins(twisted veins)
S/S of Edema
dry tight skin, brownish discoloration, venous ulcers
CVI factors
Age, inherited predisposition, obesity, pregnancy, poor muscle tone from immobility
Thrombophlebitis
inflammation and swelling of vein from clot(DVT)
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
Pulmonary Embolism S/S
Can occur due to DVT
chest pain
SOB
hemoptysis
shock
Treating venous probs (DVT,PE)
mobility
hydration
elevate legs
blood thinners
Systolic pressure
Diastolic pressure
-Pressure on arteries when heart is contracting and ejecting blood
-Pressure when heart is resting
Good perfusion
110/60, pulses can be felt, palpable arteries, nail blanching, normal organ function
Arteriosclerosis
chronic disease of arterial system
Arteriosclerosis etiology
HTN, smoking,diabetes, infectin, high cholesteral, microscopic damage,
Atherosclerosis
fat deposits in wall causing inflammation and coagulatory response
Patho of aterio disease
Ischemic pain(increase with exertion)
pale,cool skin
delayed healing
altered level of consciousness
Peripheral arterial disease (PAD)
commonly applies to legs but any arterial disease outside of the heart
Venous thrombi
Block flow toward heart
Etiology for Hypertension
Atherosclerosis
Overactive sympathetic nervous system
Overactive RAAS
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
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)
hematuria
blood in urine due to high pressures
proteinuria
protein found in urine due to high pressure
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
Aneurysm S/S
if leaks or ruptures in brain
weakness on one side of the body
change in level of consciousness
headache
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
RUQ contains
liver&gall bladder, part of pancreas, part of transverse colon
LUQ contains
part of stomach, spleen, part of transverse colon
RLQ contains
cecum, appendix, part of ascending colon
LLQ contains
Part of descending colon, sigmoid colon
Umbilical region contains
lower duodenum, jejunum, ileum
epigastric area contains
pyloric area of stomach, duodenum, art of pancreas
Gastroesophageal reflux disorder (GERD)
reflux of hydrochloric acid and pepsin from stomach into esophagus--due to relaxation of lower esophageal sphinctor
Barrett's esophagus
Tissue in esophagus becomes dysplastic (precancerous) due to GERD
Hiatal heria
stomach herniates through the diaphragm causing GERD, dysphagia (difficulty swallowing)
Gastritis
inflammation of gastric tissue can cause erosion
S/S pain, burning, bleeding
acute gastritis
results from overuse of NSAIDS (suppress protective prostaglandins) or ETOH (alcohol)
heals once offending agent is removed
Chronic gastritis (atrophic gastritis)
Autoimmune etiology
occurs in elderly
DEVELOP pernicious anemia
Peptic Ulcer disease (PUD)
inflammation of stomach and proximal duodenum mucosal lining allowing acid to ulcerate underlying tissue causing ULCERS
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
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
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
Inflammatory bowl disease
inflamm of lining and walls of intestines
Crohn's disease
ulcerative colitis
Fistula
abnormal channels or connection of organs
Crohn's disease (small intestines)
Transmural involvement (all layers of bowl are inflamed )
Patchy pattern
S/S malabsorption, bloody diarrhea, abdominal cramps, weight loss
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
Patho of an intestinal obstruction
Obstruction- buildup of fluid and gas proxima; to obst.- adbominal distention
S/S colicky abdominal pain
constipation
causes of bowl obstruction
adhesions (scaring)
hernia
tumor
intussusception ( telescope portion of bowel cutting blood)
volvulus (tortion)
paralytic ileus (loss of motion)
Paralytic illus caused by
post anesthesia, abdominal surgery. electrolyte imbalance, spinal trauma
Diverticulum/ diverticulosis
herniation of mucosa from muscle layer of intestine protruding out
No symtoms
Diverticulitis
inflammation and pain of diverticula
S/S LLQ pain, feve, leukocytosis
abscess formation, rupture
TX increase fiber, avoid seeds/nuts, anitbiotics'
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)
LGI
bleeding from lower GI
jejunum, ileum. colon
IBD, diverticulitis, neoplasms
Hematochezia
blood in the stool
Jaundice
alteration in bilirubin cycle where it gets deposited in various places manifesting as yellow-green skin
Prehepatic, hepatic, posthepatic
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
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
Hepatic jaundice
increased unconj bili from cirrhosis or hepatitis so liver cannot conjuate and conjuate bili is low
Prehepatic Blood test
bili serum- high
Indirect (unconjugated bili)- high
direct bili-normal
posthepatic blood test
bili serum- high
Indirect (unconjugated bili)- normal
direct bili- high
hepatic blood test
bili serum-high or norm
Indirect (unconjugated bili)- high
direct bili-low
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
Acute Pancreatitis
escape of pancreatic enzyme into pancreas and surrounding causing AUTODIGESTION
Pancreatic cancer
S/S pain, jaundice, weightloss
Hepatits
inflammation of the liver from autoimmune probs, microbs, idiopathic
S/S aching, fatigue, malaise, Nausea, vomiting, jaundice
viral hepatitis
HAV,
fever, malaise, jaundice
mild transmitted externally (oysters)
HBV, HCV,
transmitted parenterally (outside gut)
IV abuse, recieving blood, sexually
insidious
Cirrhosis
end stage irreversible liver disease
MAinly from alcohol abuse
toxic reaction to drugs
viral hepatitis
primary bili cirrhosis
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
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
Asterixis
liver flap-- flapping tremor of hands as result of cirrhosis
Ascites
increased back pressure into portal veins-increased hydrostatic pressure- fluid into abdominal cavity
Splenomegaly
shunting of blood into splenic vein enlarges spleen
develops hypersplenism (breakdown of RBC, WBC, thrombocytes
Varices
enlarged, thin walled veins
worse in esophagus bc it can easily rupture and bleed to death
Tests for Cirrhosis
check bilirubin levels
elevated serum liver enzymes check
Treatment for liver disease
enhance nutrition, no alcohol,
give diuretics to move T-B
IV albumin
control ammoina
protect against infection, trauma,
liver transplant
WHen HR is faster than normal
SNS fight or flight (epinephrine secreted binds to beta receptors)
Hyperkalemia causing hyopolarization
SA, AV node glitches