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78 Cards in this Set

  • Front
  • Back


(too many hormones released): suppressor test


( not enough hormones released): stimulation test

anterior pituitary

releases ACTH to adrenal cortex ; designated - releasing of hormones here

growth hormone

liver to release other hormones to develop bone and muscle growth


Secretes releasing hormones to the pituitary, tell pituitary to release their hormones, stored hormones into systemic circulation, either go to target cell or do job it is supposed to do; gets messages from the nervous system


Attach to receptors that are on the surface of the cell or on the membrane or inside the cellWill only respond if it has a receptor for a specific hormone


hormone released from a cell and acts on itself (insulin)


released from a particular cell and acts on a nearby cell

hepatic cells

synthesize bile and release into canaliculus

Hep A

Usually benign and self limiting (least virulent)Contracted primarily via fecal oral route

Does not cause chronic hepatitis or induce a carrier state

Hep B

Can be acute, chronic, carrier, lead to cirrhosis

Participates in the development of HDV

Longer incubation than Hep A and more serious

Transmitted via infected blood & body secretions

Hep C

Multiple genotypes & subtypes Common cause of chronic hepatitis, cirrhosis, end stage liver disease, liver cancer

Transmitted via infected blood & body secretions

Risks: recreational injection, high risk sexual behavior, needle sticks in the healthcare setting


Which is the least virulent strain of hepatitis?

acute liver failure

Systemic inflammation, jaundice, high blood ammonia, cerebral edema, drowsiness, slurred speech

alcoholic hep

Liver inflammation and necrosis of liver cellsIntermediate stage between fatty liver and cirrhosis

Rapid onset of jaundice

Liver tenderness, pain, anorexia, ascitesAlways serious, sometimes fatal

Progression to cirrhosis in 1-2 years

alcoholic cirrhosis

Small nodules on the liver

Fibrous scar tissue blocks sinusoids and bile canaliculi

End-stage alcoholic liver disease

non alcoholic liver disease

fatty liver disease with potential for progression to cirrhosis and end stage liver disease arising from a cause other than alcohol


Normal liver tissue replaced by fibrous (scar) tissue (irreversible)

portal hypertension

Fibrous bands increase resistance to blood flow in portal venous system (increases pressure)


Impaired bile flow

Obstructive or metabolic

Accumulation of bile in liver

Accumulation of bilirubin, cholesterol, bile acids in blood

acute pancreatitis

Acute: reversible inflammation of the pancreas (often from early activation of pancreatic enzymes)

chronic pancreatitis

progressive & permanent destruction of the exocrine pancreas, fibrosis, and later the endocrine pancreas (irreversible)

tertiary disorder

abnormality in stimulation from hypothalamus

secondary disorder

abnormality in stimulation from pituitary

primary disorder

abnormality in target gland


hypersecretion of GH in adulthood


hypersecretion of GH before puberty

acute renal failure

Rapid decline in kidney function (develops over hours/days


damage to structures within the kidney


marked decrease in renal blood flow


obstruction of urine outflow


Which type of ARF would most likely accompany benign prostatic hypertrophy?


Irreversible deterioration of renal function: permanent loss of nephrons decline in function kidney failure


best measure of overall function

Normal = 120-130 mL/minute

GFR varies with age, sex, ethnicity, body size

Measured via serum creatinine


Detrusor muscle contracts

Internal sphincter relaxes

External sphincter relaxes

flaccid bladder

absent contractions, failure to empty urine


Difficulty swallowing


autoimmune disease – causes fibrous replacement of tissues in the muscularis layer of the GI tract


Impaired muscular contraction in lower esophagus

Lower esophageal sphincter does not relax

esophageal diverticula

Out pouching of esophageal wall

Mallory Weiss Syndrome

Longitudinal tears in mucosal layer

hiatal hernia

Protrusion of stomach through esophageal hiatus


Esophageal damage caused by reflux of stomach acid

acute gastritis

Inflammation of stomach lining

Allows digestive acid to irritate stomach

chronic gastritis

Leads to atrophy of gastric epithelium

Occurs slowly over time

H Pylori

Bacteria produce enzymes/toxins that inflame & destroy mucosa of stomach

Peptic Ulcer Disease

Ulcers in lining of stomach/duodenum

irritable bowel syndrome

Chronic and recurrent intestinal symptoms not explained by structural or biochemical abnormalitiesIncreased motility & abnormal intestinal contractions

inflammatory bowel disease

Crohn disease

Autoimmune disorder

Immune response to normal (microbial) flora

Involves distal small intestine and proximal colon (can affect any area of the GI tract)

Sharp demarcated granulomatous lesions

ulcerative colitis

Autoimmune disorder

Chronic inflammation

Involves colon & rectum

Pinpoint mucosal hemorrhages, ulcerations


Persistent diarrhea with blood & mucus

infectious entercolitis

Microbes infect & inflame small intestine or colon


Pouches in colon wall (diverticula)


Infection & inflammation of diverticula


Inflamed, swollen, & gangrenous appendix


Infection or irritation of peritoneum


Triggered by gluten-containing grains

Inappropriate T-cell-mediated immune response

Type IV hypersensitivity


hormone released from pancreas when blood sugar is low


glucose synthesis in liver from a non carbohydrate

alpha cells

Produce glucagon In response to low blood glucose

beta cells

Produce insulin

Release insulin in response to spike in blood glucose

delta cells

Produce somatostatin

PP cells

Produce Pancreatic Polypeptide (PP)

Regulates pancreatic secretion

Suppresses glucagon and insulin secretion

**Decreased by the presence of somatostatin


Inhibits release of insulin

Increases glycogenolysis


Increases gluconeogenesis


Which pancreatic hormone decreases blood glucose levels?

Type 1 DM

beta cell destruction

Pancreas does not produce insulin

Predominantly an autoimmune disorder

Type 2 DM

beta cell dysfunction with insulin resistance

Pancreas does not produce enough insulin

Cells do not use insulin properly

gestational DM

Hyperglycemia in pregnant woman (without prior DM diagnosis)

Beta cells

Release: C-Peptide- helps prevent nerve and vascular damage from hyperglycemia


Excessive urination


increased thirst; because of the excessive urination

Fasting Plasma Glucose Test

Not eating before test

Casual Test

come on whenever to test blood sugar

Oral Glucose Tolerance test

75 mg of oral glucose solution, wait 2 hours x3 and check blood sugar

capillary glucose monitoring

cap test with needle

A1C test

blood test and looks at red blood cells and gives average of blood sugar for the past 3 months (want between 4-9 and below 7)


Diabetic, high level of ketones(fruity breath), acidosis- most common in type 1 diabetics

Nausea, vomiting, frequent urination, thirst, dehydration, acidosis

Ketones - byproduct of the breakdowns of fat*** Turn blood acidotic

test DKA by

Do an ABG to diagnose or test blood glucose or serum ketones