Dr. Ahangari PCB3703C Exam 1

Important material for Human Physiology Exam 1 (Dr. Ahangari) from powerpoints, lecture notes, and SG review

excess dopamine (basal ganglia)

false pleasure feeling, hallucination (i.e. cocaine)

dopamine (hypothalamus)

prolactin inhibitor

serotonin

mood, sleep, appetite

serotonin deficiency

depression, bipolar disorder

GABA

inhibitory (stimulates Cl- channels); cell relaxation phase

glycine

inhibitory (stimulates Cl- channels)

excess histamine (stomach)

excess HCl, gastritis

acetylcholine (ACh)

muscle contraction (neuromuscular junction), motility of GI tract, increases GI tract hormone secretion

ACh deficiency

muscle weakness

epinephrine & norepinephrine

control blood pressure, maintain blood glucose concentration; act as both NT and hormone

norepinephrine

relaxes smooth muscle of bronchi, decrease GI tract and urinary bladder motility

dopamine deficiency (prefrontal lobe)

social behavior and problem-solving disorders

dopamine deficiency (hypothalamus)

hyperprolactinemia → infertility (males & females)

hyperprolactinemia

dopamine deficiency in hypothalamus

typically in men and non pregnant women (prolactin naturally increases in pregnant women)

prolactin increases only in _____ _______:

suppresses _______ and ________

prepares _________ glands for ____________

pregnant women; menstruation, ovulation; mammary, breastfeeding

dopamine deficiency (brainstem)

Parkinson’s Disease (tremors, etc.)

excess dopamine (brainstem)

schizophrenia

substantia nigra

controls movement of smooth muscle, hands

serotonin deficiency treatment

more sunlight

histamine (skin)

vasodilator

histamine (lungs)

bronchoconstrictor

histamine (stomach)

increases HCl secretion

excess histamine

allergic reaction, gastritis, bronchospasms in asthmatic patients

excess ACh

gastritis

glutamate

memory & learning, Na channels

pheochromocytoma treatment

remove tumor

hyperprolactinemia treatment

bromocriptine/dopamine

hypertension, excess sweating, palpitation treatment

propranolol/NE (norepinephrine) receptor blocker

asthma treatment, NE agonsit

albuterol

gastritis (due to high histamine) treatment

histamine receptor blocker, Cimetidine

excess norepinephrine & epinephrine

pheochromocytoma: excess sweating, hypertension, headache, palpitations, constipation (in GI tract), hyperglycemia (epinephrine)

Clinical Case 1:

25 y.o. male

symptoms: obesity, sleep disorder, memory disorder, erectile dysfunction, decreased libido

NT involved?

dopamine deficiency (hypothalamus)

Case 2:

25 y.o. female

symptoms: irregular menstruation, irregular ovulation, decreased appetite, severe depression and anxiety, sleep disorder

Diagnosis? NT involved? Side effect?

hyperprolactinemia; dopamine deficiency (hypothalamus); infertility

Case 3:

65 y.o. male

symptoms: severe tremors, depression, speech disorder, motor disorder (especially walking)

NT involved?

Parkinson’s; dopamine deficiency in brainstem (substantia nigra)

Case 4:

45 y.o. female

symptoms: frequent urination, obesity, hypertension; blood test shows normal RBC, WBC, increased glucose (350 mg/dL)

Diagnosis? Treatment? If not treated in time, what are the side effects of having glucose in urine?

Diagnosis: Hyperglycemia & glucosuria; Type 2 diabetes (insulin resistance)

Glucosuria side effects: increased osmotic pressure, osmotic diuresis, excessive urination (polyuria), dehydration → excessive thirst, electrolyte loss, fatigue, nephropathy, renal failure

Treatment: diet, exercise, metformin

Case 5:

symptoms: excess sweating, hypertension, heart palpitations, hyperglycemia

diagnosis? NTs involved?

pheochromocytoma; excess NE and epinephrine

galactosemia is caused by what?

galactose-1-phosphate uridylyl transferase deficiency

galactosemia symptoms

destruction of liver & ovaries, kidney failure, mental retardation, cataracts, severe diarrhea (losing vitamins and electrolytes)

galactosemia: ______-1-phosphate uridylyl transferase ____ → accumulation of _____ → destroying, irritation of _____ _____ → destroys ___, _____, and ______

galactose; deficiency; galactose; internal organs; liver, ovaries, kidneys

marasmus

severe protein deficiency

marasmus symptoms

melanocytes are affected - skin becomes dry and fragile, atrophied muscles, weak immune system, severe diarrhea, electrolyte imbalance, hormones deficiency (mainly protein hormones - insulin, prolactin)

marasmus treatment

gradual feeding

atherosclerosis

cholesterol accumulation in blood vessels

atherosclerosis: a ____ disorder: accumulation of _____ underneath endothelial (?) layer in ____ of _____ ______ → _____ blood flow → can lead to heart attack or _____

lipid; cholesterol; walls; blood vessels; decreases; stroke

atherosclerosis main symptoms

myocardial infarction (heart attack) (if in cardio arteries) & stroke

ketone body

RESULT of 3 fatty acids: acetoacetate, acetone, & B-hydroxybutyrate

great source of energy for cells

Type I diabetes

hyperglycemia due to insulin production deficiency

Type II diabetes

hyperglycemia due to insulin resistance

Type I diabetes: _________ disease: IGG (____) destroys beta (____-producing) cells in ______ → _____ deficiency → hyperglycemia (excess _____ in blood)

AUTOIMMUNE; antibody; insulin, pancreas; insulin; glucose

Type I diabetes symptoms

vasculopathy: accumulation of glucose in vessels destroys vessel walls

neuropathy: nerves starve bc they’re glucose deprived → destroys nerves

glucosuria: blood glucose over 300mg/dl → glucose in urine

polyuria: frequent urination

polydipsia: frequent thirst

dehydration, nephropathy, proteinuria, kidney failure, hypertension

ketonuria: glucose can’t get into cell → ketone bodies in urine

*WEIGHT LOSS*

ketoacidosis, cardiovascular disorder

renal disorder, lungs release ketone bodies

Type I diabetes treatment

insulin replacement (subdermal or intravenous, IV is faster)

Type II diabetes: ____ receptor has issues → can’t reach ___ ____ → hyperglycemia

insulin; target cell

Type II diabetes symptoms

same as Type I EXCEPT patient GAINS weight (obesity risk)

Type II diabetes treatment

exercise, diet (avoid carbs, sugar, etc.), metformin

Gestational diabetes: during _____ → big change in ____ levels → risk for Type _

pregnancy; hormones; II (2)

Gestational diabetes treatment

no carbs, sugar, salty food

usually disappears after pregnancy

cofactors

accelerate enzymatic reactions

synthetic prostaglandins treat

erectile dysfunction patients

synthetic prostaglandins can also be used to

dilate cervix during labor (Pitocin)

PGE2 stimulates ____ factor → activates ____ → PGE2 level _____ → ______ body ____ and causes ____

growth; enzyme; increases; raises, temp, fever

prostaglandin’s role in menstruation:

prostaglandin → _____ accelerates rupture of ____ ____ → causes ____ → may irritate _____ _____ (main cause of _____ _____)

vasodilation, blood vessels; bleeding; sensory nerves, menstrual cramps

coenzymes

transport electrons and H ions from cytoplasm into mitochondria for ATP production

aerobic respiration: cell receives ____ molecule → last molecule, used for ___ _______ from _____ in the ______

oxygen; ATP production, glucose, mitochondria

glycolysis: target cell uptakes ____ from blood into cell → breaks down the _____ → converts into _ ______ ______

glucose; glucose; 2 pyruvic acids

product of glycolysis

2 pyruvic acids!!!

glucose formula

C6H12O6

pyruvic acid formula

C3H4O3

how many H are left in the cytoplasm of target cell in mitochondria for ATP production

4 (12H from glucose - 8H from both pyruvic acids)

what happens to the H ions after glycolysis

2 disappear, 2 are gained by NAD-coenzyme

= reduction!!

lactic acid

tissue doesn’t have sufficient oxygen supply

lactic acid: insufficient ____ to target cell → ____ ____ can’t get into _____ for ___ production & Krebs cycle → _____ _____ stays in cytoplasm → lactic acid

oxygen; pyruvic acid, mitochondria, ATP; pyruvic acid

lactic acid formula

C3H6O3

myocardial infarction

atherosclerosis keeps myocardium from getting sufficient oxygen → lactic acid

ischemia

deficiency of oxygen supply OR increased blood oxygen level, harmful to cells (i.e. heart attack, stroke)

glycogenesis

liver uptakes extra glucose from digestive system → converts into glycogen

glycogen is for

storage in the liver

glycogenolysis

when body needs more glucose, liver breaks down and converts glycogen to glucose → great source of glucose to other organs, skeletal muscle

gluconeogenesis

liver uptakes lactic acid, fatty acid, amino acids, and glycerol → converts into (new) glucose

Cori cycle

liver converts old things into new glucose, releases into blood → new glucose taken into muscle

coenzymes

FAD & NAD