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162 Cards in this Set

  • Front
  • Back
Necrosis
Non-programmed cell death. Inflammation, nucleus destroyed first
Apoptosis
Programmed cell death. No inflammation, nucleus guides death destroyed last
Pyknosis
nucleus turn into blobs " pick blobs"
Karyorrhexis
Nucleus fragments
Karyolysis
Nucleus dissolves
Somatotrope
GH
Gonadotrope
LH, FSH
Thyrotrope
TSH
Corticotrope
ACTH
Lactotrope
PRL- Prolactin
What receptors do protein hormones use?
cell membrane receptors
What receptors do steroid hormones use?
nuclear membrane receptors
What are the steroid hormones?
"PET CAD"
Progesterone
E₂ (Estradiol)
Testosterone
Cortisol
Aldosterone
What does endocrine mean?
secretion into the blood
What does exocrine mean?
secretion into non-blood
What is autocrine?
works on itself
What is paracrine?
Works on its neighbor
What is Merocrine?

Example:
cell is Maintained => exocytosis
What is apocrine?
Apex of the cell is secreted
What is holocrine?
the whole cell is secreted
What organs do not require insulin?
"BRICKLE"
Brain
RBC
Intestine
Cornea,Cardiac
Kidney
Liver
Exercising muscle
What is the function of GnRH?
stimulates LH , FSH
What is the function of GRH
stimulates GH
What is the function of CRH
stimulates ACTH
What is the function of TRH
stimulates TSH
What is the function of PRH?
stimulates Prolactin (PRL)
What does Dopamine does?
inhibits prolactin
What is the function of SS?
inhibits GH
What is the function of ADH
conserves water, vasoconstrics and concentrate urine
What is the function of oxytoxin?
milk let down, baby let down
What does GH do?
IGF-1 release from liver
What is the function of TSH?
T₃ and T₄ release from thyroid
What is the function of LH?
Testosterone release from testis, E₂ and progesterone release from ovary
What is the function of FSH?
sperm or egg growth
What is the function of PRL?
milk production
What is the function of ACTH?
stimulates cortisol and androgn release from adrenal gland
What is the function of MSH
Provides skin pigmentation
What are the stress hormones and do they appear?
Epinephrine: 20 minutes
Glucagon: 20 mins
Insulin: 30 min
ADH: 30 min
Cortisol: 2-4 hr
GH: 24hr
What is the function of ADH? ffffff
concentrates urine, vasoconstriction and conserves water
What is diabetes insipitudus?
presentation of the patient
too little ADH => urinate a lot
What is Central (neurogenic) diabetes insipitudus?
Brain not making or producing enough ADH
What is nephrogenic diabetes insipitudus?
Which drugs can cause this?
ADH receptor (V2 aquaporin) is blocked or broken.

Can be cause by Lithium and Demecocycline
What does the water deprivation tell you?
If patient fails to concentrate urine they have diabetes insipitudus
What does giving DDAVP (vasopresin) during water deprivation tell you?
DDAVP => Central complete DI (concentrates >50 %)
DDAVP => Central partial DI (concentrates 10-50 %)
DDAVP => nephrogenic DI (no change)
What is SIADH?
What happens to plasma volume
What does this lead to?
too much ADH => expand plasma vol =>pee Na
What is the difference in urine concentration between DI and SIADH?
DI has dilute urine, SIADH has concentrated urine
What is psychogenic polydipsia?
describe the plasma osmolarity
pathologic water drinking => low plasma osmolarity
What does aldosterone do?
reabsorbs Na and 3 water and secretes H+/K+
What is a neuroblastoma?
presentation:
lab:
adrenal tumor in kids
dancing eyes and feet
secretes catecholamines
What is a pheochromocytoma?
presentation:
lab:
adrenal medulla tumor in adults,
perspiration, palpitation, pain, pressure, pallor (5P's)
secretes catecholamines
What does the zona glomerulosa make?
aldosterone "salt"
What does the zona fasiculata make?
cortisol "sugar"
What does the zona reticularis make?
androgens "sex"
What does ANP do?
Inhibits aldosterone, dilates renal artery (afferent arteriole)
What does calcitonin do?
Inhibits osteoclast => low serum Ca₂⁺
What is Multiple endocrine neoplasia MEN I?
name
"Wermer's 3 P's: Pancreas, Pituitary, Parathyroid adenoma
What is Multiple endocrine neoplasia MEN II (2A)?
"Sipples": Parathyroid adenoma (PTH), Medullary carcinoma of the thyroid, Pheochromocytoma,
What is Multiple endocrine neoplasia MEN III (2B)?
MEN IIb: Marfanoid body habitus, GI mucosal neuromas, Medullary carcinoma of the thyroid, Pheochromocytoma,
What does CCK do?
gallbladder contraction, bile release
What does cortisol do?

What does this lead to?
gluconeogenesis by proteolysis => thin skin
Define conn's syndrome

What test will make it worse?
high aldosterone tumor

Captopril test makes it worse
What is Addison's disease?

What does this lead to?
Autoimmune destruction of adrenal cortex. Leads to ⇧ACTH and hyperpigmentation.
what is Waterhouse Friderichsen Syndrome?
What is another name for WFS?
Adrenal hemorrage most commonly due to meningococcus Neisseria Meningitidis

Also know as Hemorragic adrenalitis or Fulminant meningococcemia
What is Cushing's disease?

What is Cushing's syndrome?
Cushing's disease:
high ACTH due to pituitary tumor

Cushing's syndrome:
Hight cortisol produced from a pituitary/Adrenal tumor or small cell CA
Nelson's syndrome
hyperpigmentation after adrenectomy and visual problems
If low-dose dexamethasone test suppresses, what does that tell you?
Patient is either depressed, obese, or it's a normal variant
If low-dose dexamethasone test does not suppresses, what does that tell you?
Management?
Patien has Cushing's tumor, Then do a high-dose dexamethasone test next


=> ACTH (call a brain surgeon)
If high-dose dexamethasone test does suppress, what does that tell you?

If high-dose dexamethasone test does not suppress, what does that tell you?
Pituitary adenoma => ACTH (call a brain surgeon)

Adrenal adenoma => cortisol is high (call general surgeon)
small cell lung cancer => ACTH (call thoracic surgeon)
what are the survival hormones?
cortisol: permissive under stress
TSH: permissive under normal
What does epinephrine do?
gluconeogenesis, glycogenolysis
What does erythropoetin do?
makes RBC's
What does gastrin do?
stimulates parietal cells => IF, H+
What does growth hormone do?
growth, sends somatomedin to growth plates, gluconeogenesis by proteolysis
What is pygmie?
no somatomedin receptors
What is achondroplasia (Laron Dwarf)?
abnormal FGF receptors in extremities
What is midget?
decreased somatomedin receptor sensitivity
What is acromegaly?
presentation (5)
increase of what hormone?
adult bones stretch "my hat doesn't fit,
coarse facial features, large furrowed tongue
deep husky voice, jaw protution

increase IGF-1 b/c of GH tumor.
What is gigantism?
childhood form of acromegally
What does GIP do?
What does it lead to?
Enhance insulin action responsable for post prandial hypoglycemia
What does glucagon do?
Gluconeogenesis, glycogenolysis, lipolysis, ketogenesis
what does insulin do?
pushes glucose into cells
what is type I Diabetes Mellitus?
Etiology (3):
Presentation:
anti-islet antibodies, Glutamic acid decarboxylase antibody (GAD Ab), coxsakie B infection, low insulin, DKA, polyuria, polydipsia, polyphagia
What is type II Diabetes Mellitus?
presentation
neck
Insulin receptor insensitivity (high insulin)
Hyper osmolar non-etotic coma (HONK)
Acanthosis nigricans
How does DKA present?
kaussmal respirations, fruity breath (acetone), altered mental status
Treatment for DKA?
Insulin, NS, KCl, D5 1/2 NS
What is dawn phenomenon? Tx
morning hyperglycemia due to GH
Tx: increase pm insulin
What is somogyi effect?
Tx:
morning hyperglycemia due to evening hypoglycemia.
Tx: decrease pm insulin
What is factitious hypoglycemia?
what are the insulin and c-peptide levels
insulin injection (increase insulin, decrease c-peptide)
What is insulinoma?
tumor (increase insulin, increase c-peptide)
What is erythrasma?
test
tx:
rash in skin folds
Test: Coral red under wood's lamp
Tx: erythromycin
What is syndrome X = metabolic syndrome? tx:
"Pre DM" => HTN, dyslipidemia, hyperinsulinemia, acanthosis nigrans
tx: metformin
What are the foot ulcer risk factors?
DM/ Poor Glycemic control (HbA1c>7)
Smoker
Bony abnormalities
Previous ulcers
What are the 5 conditions causes weight gain?
obesity
hypothyroidism
depression
cushing's
anasarca
What does motilin do?
stimulates segmentation which is primary peristalsis and migrating motor coplex (MMC)
What does PTH do?
Simulates osteoblast to activate osteoclast (chews up bone)
What does vitamin D do?
Help in calcium reabsorption from the GI tract (builds bone)
what does the parathyroid chief cells secrete?
PTH
What do stomach chief cells secrete?
pepsin
what is the difference between Norepinephrine and epinephrine
norepinephrine is a neurotransmitter and epinephrine is a hormone
What diagnosis has primary hyperparathyroidism?
parathyroid adenoma
What diagnosis has secondary hyperparathyroidism?
renal failure
What is familial hypocalciuria hypercalcemia?
decrease calcium excretion
What disease process present when both serum calcium and PO⁴ are decreased?
Vitamin D deficiency
What type of problem is there if serum calcium and PO⁴ change in opposite directions?
PTH problem (secondary)
high Ca => hyperPTH
low Ca => hypoPTH
What is the most common cause of primary hypoparathyroidism?
thyroidectomy
what is pseudohypoparathyroidism?
what is decreased?
bad PTH receptor on the kidney
decreased urinary cAMP
What is pseudopseudohypoparathyroidism?
G-protein defect, no Ca₂⁺ problem
What is hungry bone syndrome?
Remove PTH and the bone sucks in Ca₂⁺
What does secretin do?
Secretion of bicarbonate, inhibits gastrin, and tighten pyloric sphincter
What does somatostatin do?
Inhibits secretin, motilin, CCK
What do T₃ and T₄ do?
growth and differentiation
What disease has exophthalmos?
Grave's disease
What disease has enophthalmos?
Horner's, Marfan's
What does oxytocin do?
milk ejection, baby ejection
What does PRL do?
milk production
What are the 5 hyperthyroid diseases?
Grave's
DeQuervain's
Silent thyroiditis
Plummer's
Jod-basedow
What do you see in Grave's disease?
Exopthalmos, pretibial myxedema, anti-TSH receptor antibodies
What do you see in DeQuervain's disease?
viral origin, painful jaw, hypo and hyperthyroid symptoms
What do you see in silent thyroiditis ?
post-partum patiens
What would you see in Plummer's disease?
patiens with benign adenoma and or patiens over 50 years old
What is Jod-basedow disease?
transient hyperthyroidism due to increased Iodine
What are the 5 hypothyroid diseases?
Hashimoto's
Reidel's struma
Cretinism
Euthyroid sick syndrome
wolff-chaikoff
Hashimoto's antibodies
antimicrosomal Ab =TPO Ab
What is Reidel's struma?
Woody connective tissue in the neck. Death due to suffocation. Rule out cancer
What is Cretinism?
mom and baby are hypothyroid. Features in the whrong place. Will have dietary problems.
What is Euthyroid sick syndrome?
low T₃ syndrome. Decrease convertion of T4 to T3
What is Wolff-Chaikoff?
transient hypothyroidism
What is Plummer's syndrome?
Hyperthyroid adenoma
What is plummer-vinson syndrome?
esophageal webs
What does testosterone do?
Makes external male genitalia
What does mullerian Inhibiting factor (MIF) do?
Inhibits formation of female internal structures
What does thyroid peroxidase (TPO) and thymosin do?
Help T cells mature
what does vosoactitive interstitinal peptide (VIP) do?
inhibit secretin, motilin, CCK. Opens sphincters.
How does a VIPoma present?
Watery diarrhea
How does a SSoma present?
Constipation
What are the hormones with disulfide bonds?
"PIGI"
Prolactin
Inhibin
Growth hormone
Insulin
Which hormones have the same α subunits?
LH, FSH
TSH
β-HCG
Which hormones produce acidophils?
"GAP"
GH
PRL
What hormones produce basophils
"B FLAT"
FSH
LH
ACTH
TSH
Treatment strategy for type l DM
low-sugar diet, insulin replacement.
Treatment strategy for type lI DM
dietary modification and exercise for weight loss; oral
hypoglycem ics and insulin replacement
What is the mechanism of action of insuline?
Bind insulin receptor (tyrosine
kinase activity). Pushes k+ into the cell

Liver: increase glucose stored as glycogen. Increase triglyceride synthesis
Muscle: increase glycogen and protein synthesis, K+ uptake.
Fat: improves TG storage by activating Lipoprotein Lipase. Decrease circulating free fatty acids.
What are the indication for insuline?



What is the adverse effect of insuline?
CLINICAL USE:
Type l DM, type 2 DM, gestational diabetes, lifethreatening hyperkalemia, and stress-induced
hyperglycemia.

Adverse effect of insuline:
Hypoglycemia, very rarely hypersensitivity reactions.
Insulin :
Which are the rapid-acting insuline?
Which are the short-acting insuline?
Which are the intermediate acting insuline?
Which are the long acting insuline?
Lispro (rapid-acting)
Aspart (rapid-acting)
Glulisine (rapid-acting)

Regular (short-acting)

NPH (intermediate)

Glargine (long-acting)
Detemir (long-acting)
Ultralente (long-acting)
What is the mechanism of Sulfonylureas?
Close K+ channel in the pancreatic beta cell membrane , so cell depolarizes
--> triggering of insulin release via
increase Ca2+ influx.
What are the first generation Sulfonylureas?
What are the indications for Sulfonylureas?
First generation :
Tolbutamide
Chlorpropamide

NIDDM (type 2) Stimulate release of
endogenous insulin in type
2 DM.
What are the second generation Sulfonylureas?
What are the indications for Sulfonylureas?
Second generation :
Glyburide
Glimepiride
Glipizide

NIDDM (type 2) Stimulate release of
endogenous insulin in type
2 DM.
Clinical use of Sulfonylureas?
Function of what cells is necessary for the action of Sulfonylureas?
Stimulate release of endogenous insulin in type
2 DM.
Requires some islet cell function so drug is useless in Type 1 DM
What are the adverse effect of Sulfonylureas?
First generation : disulfiram like effects.

Second generation :
Less side effects: hypoglycemia GI disturbances, muscle weakness, mental confusion
Which are the Biguanides:
Mechanism of action
Indications
Adverse effect of biguanides:
Metformin
Exact mechanism is unknown. Decrease gluconeogenesis, Increase glycolysis, increase peripheral glucose uptake (insulin sensitivity).

Oral. First-line therapy in type 2 DM. Can be used in patients without islet function.

GI upset; most serious adverse effect is
lactic acidosis (thus contraindicated in renal failure). Stop use in patients undergoing studies using Contrast
Which are the Glitazones/Thiazolidinediones drugs?
1) Mechanism of action:
2) Indications:
3) Adverse effect:
Pioglitazone and Rosiglitazone
1) Mechanism of action:
increase insulin sensitivity in peripheral
tissue. Binds to PPAR-gamma nuclear transcription regulator."
2) Indications:
NIDDM (Type 2) Used as monotherapy in type
2 DM or combined with DM agents.
3) Adverse effect:
Weight gain, edema. Hepatotoxicity; increase LDL and triglycerides, heart failure.
Which are the Alpha-glucosidase inhibitors drugs?
1) Mechanism of action:
2) Indications:
3) Adverse effect:
Acarbose; Miglitol
1) Mechanism of action:
Inhibit intestinal brush-border a-glucosidases.
Delayed sugar hydrolysis and glucose absorption
from the gut. Decrase postprandial hyperglycemia
2) Indications:
NIDDM (Type 2) Used as monotherapy in type
2 DM or combined with DM agents.
3) Adverse effect:
GI disturbances and may reduce absorption of iron
Which are the Mimetrics (Amylin analogs) drugs?
1) Mechanism of action:
2) Indications:
3) Adverse effect:
Pramlintide

1) Mechanism of action:
decreases glucagon.

2) Indications:
Type l and type 2 DM.

3) Adverse effect:
Hypoglycemia, nausea, diarrhea.
Which are the GLP-1 analag (glucagon like peptide) drugs?
1) Mechanism of action:
2) Indications:
3) Adverse effect:
Exenatide Liraglutide
1) Mechanism of action:
increases insulin, decreases glucagon release.
2) Indications:
NIDDM (Type 2)
3) Adverse effect:
Nausea, vomiting; pancreatitis.
What is the mechasism of action of Growth hormone?
Indications:
Stimulates liver production of insuline-like growth factors
Indications:
GH deficiency in children, Turner syndrome; Burn victims
What is the mechasism of action of ostreotide (Synthetic analog of somatostatin)?
2) Indications:
3) Adverse effect:
Decreases release of GH, Gastrin, CCK, VIP, Glucagon, Insulin

Acromegaly, carcinoid syndrome, gastrinoma, glucagonoma, esophageal varices.
What is the indication for Oxytosin?
Induces labor; control uterine hemorrhage
What is the mechasism of action of DDAVP/ADH (desmopressin)?
What is the indication for DDAVP/ADH (desmopressin)?

Which are the adverse effects for DDAVP/ADH (desmopressin)?
1) Mechanism: Recruits water channels to luminal membrane in collecting duct
2) Indications:
Antidiuresis; Pituitary (central, not nephrogenic) DI.
3) Adverse effect:
Overhydration; alergic reaction
Propylthiouracil and methimazole
1) Mechanism of action:
2) Indications:
3) Adverse effect:
1) Mechanism of action:
Block peroxidase, thereby inhibiting organification of iodide and coupling of thyroid hormone
synthesis. Propylthiouracil also blocks 5' deiodinase, which decrease peripheral conversion of T4 to T3 .
2) Indications:
To treat Hyperthyroidism.

3) Adverse effect:
Skin rash, agranulocytosis (rare), aplastic anemia, hepatotoxicity (propylthiouracil). Methimazole is
a possible teratogen.
Demeclocycline
1) Mechanism of action:
2) Indications:
3) Adverse effect:
1) Mechanism of action:
ADH antagonist (member of the tetracycline family).
2) Indications:
SIADH.
3) Adverse effect:
Nephrogenic DI, photosensitivity, abnormalities of bone and te
Levothyroxine (T4) triiodothyronine (T3)
1) Mechanism of action:
2) Indications:
3) Adverse effect:
1) Mechanism of action:
Thyroxine replacement.

2) Indications:
Hypothyroidism, myxedema.

3) Adverse effect:
Tachycardia, heat intolerance, tremors, arrhythmias.
List the 5 most common Glucocorticoids:
1) Mechanism of action:
2) Indications:
3) Adverse effect:
Hydrocortisone, prednisone, triamcinolone, dexamethasone, beclomethasone.
1) Mechanism of action:
decrease the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression
of COX-2.
2) Indications:
Addison's disease, inflammation, immune suppression, asthma.
3) Adverse effect:
Iatrogenic Cushing's syndrome -buffalo hump, moon facies, truncal obesity, muscle wasting, thin
skin, easy bruisability, osteoporosis, adrenocortical atrophy, peptic ulcers, diabetes (if chronic).
Adrenal insufficiency when drug stopped abruptly after chronic use.