Mod 4 exam chem

Cushings and Addisons ORGAN/GLAND

Adrenal Gland

Graves Disease and hashimoto’s thyroiditis ORGAN/GLAND

Thyroid gland

Diabetes ORGAN/GLAND

Pancreas and beta cells of the islet of langerhans

Diabetes insipidus (DI) ORGAN/GLAND

Pituitary gland

Insulinomas ORGAN/GLAND

Tumors of the pancreatic islets

Rickets/Osteomalacia ORGAN/GLAND

Parathyroid gland

Cushings Hyper/Hypo

Adrenal hyperfunction

Addison’s (Primary adrenal insufficiency) Hyper/Hypo

Graves disease Hyper/Hypo

Hashimoto’s thyroiditis Hyper/Hypo

Diabetes Hyper/Hypo

Hyper

Diabetes insipidus (DI) Hyper/Hypo

Decreased ADH secretion

Insulinomas Hyper/Hypo

Hypo

Rickets/Osteomalacia Hyper/Hypo

Increased PTH

Cushings syndrom Symptoms

Fat pad (buffalo hump), stretch marks, think arms and legs, thin skin/bruising, thinning hair, red cheeks, round “moon” face

Addison’s (Primary adrenal insufficiency) Symptoms

Fatigue, weakness, weight loss, hyperpigmentation (primarily elbows, knees, knuckles), and hypotension

Graves Disease Symptoms

Heat intolerance, tachycardia, weight loss, weakness, emotional liability, and tremor ;Can have bulging eyes (exophthalmos)

Hashimotos Thyroiditis Symptoms

Bradycardia, cold sensitivity, dry skin, hair loss, brittle nails, and muscle weakness

Diabetes Symptoms

Polydipsia, polyuria, weight loss and hunger, lethargic, blurry vision

Diabetes insipidus (DI) Symptoms

Polyuria and polydipsia

Rickets/Osteomalacia symptoms

Delayed growth, delayed

motor skills, muscle

weakness, and bone pain

Cushings Lab tests

High cortisol (am sample preferred), Urinary free cortisol (24 hr), Increased ACTH

Addisons disease Lab tests

Low cortisol (am sample preferred), Low sodium, high potassium, Decreased ACTH

Graves disease Lab tests

TSH normal/decreased, T3, FT4 and T4 elevated, Ultrasound/MRI/CT

Hashimotos thyroiditis Lab tests

Increased TSH, Decreased T3 and T4, Increased anti-TPO

Diabetes Lab tests

A1C >6.5, Fasting plasma glucose >125, OGTT, 2-hour >200

Insulinomas Lab tests

Low plasma glucose, Elevated levels of insulin, Elevated levels of C-peptide

Rickets/Osteomalacia Lab tests

Vitamin D deficiency, Decreased calcium, and, phosphorous

Prehapatic Jaundice Cause

Increased production of bilirubin by the body

Hepatic Jaundice Cause

Results from a problem occurring in the liver

Post hepatic jaundice (Obstructive jaudice) Cause

Blockage of the flow of bile from the liver

Cirrhosis (irreversible liver scarring) Cause

All chronic liver diseases can progress to cirrhosis

Reyes syndrome Cause

Children recovering from viral infections who have taken aspirin

Hepatitis A Cause

Transmitted through fecal-oral route (ingestion of food, water, or objects contaminated with feces)

prehepatic jaundice symptoms

Process or disease resulting in increased hemolysis and excessive destruction of RBCs leads to increased bilirubin levels

examples: hemolytic anemia, transfusion reaction, hemolytic disease of the newborn

Hepatice jaundice symptoms

Disorders of bilirubin metabolism, cirrhosis, viral hepatitis, alcoholic liver disease, and neonatal jaundice

Post-hepatic jaundice (obstructive jaundice) symptoms

Gallbladder stones are the most common cause

Cirrhosis (irreversible liver scarring) symptoms

Portal hypertension, varices, edema, ascites, bruising, itching, and hepatic encephalopathy

Reye’s syndrome symptoms

Swelling of the liver and brain; seizures, loss of consciousness, repeated vomiting, lethargy

Hepatitis A symptoms

Clay or gray colored stool.

Jaundice, Lethargy, nausea/vomiting/diarrhea, abdominal pain, fever, dark urine

Prehepatic jaundice lab test

Increased total serum bilirubin and unconjugated bilirubin

hepatic jaundice lab test

Elevated AST and ALT

Elevated conjugated and unconjugated bilirubin

post-hepatic jaundice (obstructive jaundice) lab test

Significantly elevated conjugated bilirubin and ALP and GGT

Cirrhosis lab test

Elevated AST and ALT

Elevated bilirubin

Reyes syndrome lab test

Elevated ammonia, high liver enzymes, low glucose, prolonged (elevated) PT/INR

Hepatitis A lab test

IgM anti-HAV Ab—acute phase

IgG anti-HAV Ab—later infection (years)

Hepatitis B Cause

Transmitted through direct contact with infected blood, semen, or vaginal fluids (sexual contact, infected needles, mother to baby)

Hepatitis C Cause

Transmitted through direct contact with infected blood (infected needles, unsafe medical procedures, unregulated tattoos)

Porphyria Cause

Metabolic disorder caused by a deficiency in one of the enzymes involved in the heme biosynthetic pathway. Porphyrins build up in the liver or bone marrow.

IDA Cause

The body lacks sufficient iron to produce hemoglobin

Hemochromatosis HH Cause

Iron overload

Excessive iron absorption and accumulation in tissue

hepatitis b symptoms

Jaundice

Lethargy, nausea/vomiting, abdominal pain, fever, dark urine

hepatitis c symptoms

Jaundice; fluid buildup in the stomach area (ascites), hepatic encephalopathy, spider angiomas; Lethargy, weight loss, bruising and bleeding easily, dark colored urine

porphyria symptoms

Acute: Severe abdominal pain (most common), tachycardia and high bp, possible neurological issues and psychiatric symptoms

Porphyria cutanea tarda: skin changes (pigmentation changes, thickening, blisters on sun-exposed areas) and hypertrichosis

(excessive hair growth)

IDA symptoms

General: Fatigue, pallor, tachycardia

“Hallmark”: koilonychia (spooning nails), glossitis (inflamed tongue, pica (cravings for nonfood items)

Hemochromatosis HH symptoms

Cirrhosis, diabetes mellitus, and bronzing of the skin (due to melanin)

hepatitis B lab test

HBsAg—acute or active phase

HBcAg and HBeAg—later in theinfection

Anti-HBc is the most commonly detected antibody

Hepatitis C lab test

Anti-HCV antibody—screening

Porphyria lab test

Red or dark brown urine (often turns this color after exposure to light)

Low sodium and magnesium

Mid elevations of ALT

Iron deficiency anema IDA ab test

Decreased serum iron andferritin

Increased TIBC and transferrin

Microcytic hypochromic rbcs

Hemochromatosis (HH) lab test

Increased serum iron and ferritin

Decreased transferrin and TIBC

Microcytic anemia

Creatinine Kinase (CK)— isoenzymes clinical signigfigance

2 subunits (BB-brain; MM-muscle; MB-heart)

CK can be elevated in chronic muscle diseases, end- stage renal disease, and with extreme exercise

CKMB is cardiac specific

Troponin T (TnT) clinical signifigance

Elevated during AMI, but can also rise in chronic kidney disease or skeletal muscle conditions; Tn1 is a better biomarker than TnT

Troponin 1 (TnI) clinical signifigance

Highly specific to heart tissue; elevated levels reliably

indicate damage to the myocardium

Myoglobin clinical signifigance

Cardiac marker, but usually not utilized because it diffuses into the blood rapidly

Protein in muscle similar to hemoglobin

C-reactive protein (CRP) clinical signifigance

Acute marker of inflammation used clinically in the evaluation of CVD risk

Biomarker of atherosclerotic cardiovascular disease risk

Homocysteine clinical signifigance

Assessment of cardiovascular disease risk

Elevated levels cause arterial damage, promote inflammation, and increase the likelihood of blood clots, leading to atherosclerosis, heart attack, and stroke.

B-type natriuretic peptide (BNP) clinical signifigance

Secreted by the heart ventricles; defense against volume overload

Helpful in distinguishing cardiac from noncardiac causes of dyspnea

Creatinine Kinase (CK)— isoenzymes Expected results after AMI

Rises within 6-8 hours

Peaks by 24 hours

Returns to normal within 3-4 days

Troponin T (TnT) expected results after AMI

Rises 4-6 hours

Fall or returns to normal 4 days

Troponin 1 (TnI) expected results after AMI

Rises 4-6 hours

Fall or returns to normal 10 days

Myoglobin expected results after AMI

Rises 1-3 hours

Fall or returns to normal <1 day

Cystic Fibrosis Causes

Genetic disorder

Zollinger-Ellison syndrome Cause

Gastrin-secreting tumors

(gastrinomas) in the pancreas

or duodenum

Acute pancreatitis (sudden onset, lasts for a short period of time, and usually resolves) Cause

Alcohol and biliary tract disease or obstructive liver disease (often a gallstone)

Cystic fibrosis Symptoms

Recurrent infection withunusual pathogens; increased

inflammation of the lungs; mucus accumulation

Zollinger-Ellison syndrome Symptoms

Chronic peptic ulcers, steatorrhea, GERD

Acute pancreatitis Symptoms

Enlarged pancreas

Steatorrhea and malabsorption

Upper right abdominal pain

Vomiting

Acute pancreatitis Lab test

• Lipase and amylase are

extremely elevated (often 2-3

times the upper limit of

normal)

• Lipase (almost exclusively a

pancreatic function test)

It increases in serum within 24

hours in acute pancreatitis,

persists for 8-14 days from

reabsorption, and is not

cleared like amylase

• Amylase Serum increases within 3-6

hours of the onset of the

diseases, reaches a peak in

about 24 hours, and returns to

normal within 3-5 days

Urine is more sensitive

Zollinger-Ellison syndrome Lab Tests

Extremely elevated fasting serum gastrin

Gastric pH (extremely acidic)

Secretin stimulation tests, calcium infusion test, and imaging

Cystic fibrosis Lab Tests

Chloride sweat test (>60)

Fecal pancreatic elastase-1

Genetic testing