Patho Exam 3

(too many hormones released): suppressor test

( not enough hormones released): stimulation test

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

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

synthesize bile and release into canaliculus

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

Does not cause chronic hepatitis or induce a carrier state

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

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?

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

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

Small nodules on the liver

Fibrous scar tissue blocks sinusoids and bile canaliculi

End-stage 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)

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

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

abnormality in stimulation from hypothalamus

abnormality in stimulation from pituitary

abnormality in target gland

hypersecretion of GH in adulthood

hypersecretion of GH before puberty

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

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

Out pouching of esophageal wall

Longitudinal tears in mucosal layer

Protrusion of stomach through esophageal hiatus

Esophageal damage caused by reflux of stomach acid

Inflammation of stomach lining

Allows digestive acid to irritate stomach

Leads to atrophy of gastric epithelium

Occurs slowly over time

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

Ulcers in lining of stomach/duodenum

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

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

Autoimmune disorder

Chronic inflammation

Involves colon & rectum

Pinpoint mucosal hemorrhages, ulcerations

Pain

Persistent diarrhea with blood & mucus

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

Produce glucagon In response to low blood glucose

Produce insulin

Release insulin in response to spike in blood glucose

Produce somatostatin

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?

beta cell destruction

Pancreas does not produce insulin

Predominantly an autoimmune disorder

beta cell dysfunction with insulin resistance

Pancreas does not produce enough insulin

Cells do not use insulin properly

Hyperglycemia in pregnant woman (without prior DM diagnosis)

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

Excessive urination

increased thirst; because of the excessive urination

Not eating before test

come on whenever to test blood sugar

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

cap test with needle

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

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