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162 Cards in this Set
- Front
- Back
Necrosis
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Non-programmed cell death. Inflammation, nucleus destroyed first
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Apoptosis
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Programmed cell death. No inflammation, nucleus guides death destroyed last
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Pyknosis
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nucleus turn into blobs " pick blobs"
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Karyorrhexis
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Nucleus fragments
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Karyolysis
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Nucleus dissolves
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Somatotrope
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GH
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Gonadotrope
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LH, FSH
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Thyrotrope
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TSH
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Corticotrope
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ACTH
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Lactotrope
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PRL- Prolactin
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What receptors do protein hormones use?
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cell membrane receptors
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What receptors do steroid hormones use?
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nuclear membrane receptors
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What are the steroid hormones?
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"PET CAD"
Progesterone E₂ (Estradiol) Testosterone Cortisol Aldosterone |
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What does endocrine mean?
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secretion into the blood
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What does exocrine mean?
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secretion into non-blood
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What is autocrine?
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works on itself
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What is paracrine?
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Works on its neighbor
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What is Merocrine?
Example: |
cell is Maintained => exocytosis
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What is apocrine?
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Apex of the cell is secreted
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What is holocrine?
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the whole cell is secreted
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What organs do not require insulin?
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"BRICKLE"
Brain RBC Intestine Cornea,Cardiac Kidney Liver Exercising muscle |
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What is the function of GnRH?
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stimulates LH , FSH
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What is the function of GRH
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stimulates GH
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What is the function of CRH
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stimulates ACTH
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What is the function of TRH
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stimulates TSH
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What is the function of PRH?
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stimulates Prolactin (PRL)
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What does Dopamine does?
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inhibits prolactin
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What is the function of SS?
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inhibits GH
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What is the function of ADH
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conserves water, vasoconstrics and concentrate urine
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What is the function of oxytoxin?
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milk let down, baby let down
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What does GH do?
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IGF-1 release from liver
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What is the function of TSH?
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T₃ and T₄ release from thyroid
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What is the function of LH?
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Testosterone release from testis, E₂ and progesterone release from ovary
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What is the function of FSH?
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sperm or egg growth
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What is the function of PRL?
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milk production
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What is the function of ACTH?
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stimulates cortisol and androgn release from adrenal gland
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What is the function of MSH
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Provides skin pigmentation
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What are the stress hormones and do they appear?
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Epinephrine: 20 minutes
Glucagon: 20 mins Insulin: 30 min ADH: 30 min Cortisol: 2-4 hr GH: 24hr |
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What is the function of ADH? ffffff
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concentrates urine, vasoconstriction and conserves water
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What is diabetes insipitudus?
presentation of the patient |
too little ADH => urinate a lot
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What is Central (neurogenic) diabetes insipitudus?
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Brain not making or producing enough ADH
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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 |
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What does the water deprivation tell you?
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If patient fails to concentrate urine they have diabetes insipitudus
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What does giving DDAVP (vasopresin) during water deprivation tell you?
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DDAVP => Central complete DI (concentrates >50 %)
DDAVP => Central partial DI (concentrates 10-50 %) DDAVP => nephrogenic DI (no change) |
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What is SIADH?
What happens to plasma volume What does this lead to? |
too much ADH => expand plasma vol =>pee Na
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What is the difference in urine concentration between DI and SIADH?
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DI has dilute urine, SIADH has concentrated urine
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What is psychogenic polydipsia?
describe the plasma osmolarity |
pathologic water drinking => low plasma osmolarity
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What does aldosterone do?
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reabsorbs Na and 3 water and secretes H+/K+
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What is a neuroblastoma?
presentation: lab: |
adrenal tumor in kids
dancing eyes and feet secretes catecholamines |
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What is a pheochromocytoma?
presentation: lab: |
adrenal medulla tumor in adults,
perspiration, palpitation, pain, pressure, pallor (5P's) secretes catecholamines |
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What does the zona glomerulosa make?
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aldosterone "salt"
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What does the zona fasiculata make?
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cortisol "sugar"
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What does the zona reticularis make?
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androgens "sex"
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What does ANP do?
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Inhibits aldosterone, dilates renal artery (afferent arteriole)
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What does calcitonin do?
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Inhibits osteoclast => low serum Ca₂⁺
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What is Multiple endocrine neoplasia MEN I?
name |
"Wermer's 3 P's: Pancreas, Pituitary, Parathyroid adenoma
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What is Multiple endocrine neoplasia MEN II (2A)?
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"Sipples": Parathyroid adenoma (PTH), Medullary carcinoma of the thyroid, Pheochromocytoma,
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What is Multiple endocrine neoplasia MEN III (2B)?
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MEN IIb: Marfanoid body habitus, GI mucosal neuromas, Medullary carcinoma of the thyroid, Pheochromocytoma,
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What does CCK do?
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gallbladder contraction, bile release
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What does cortisol do?
What does this lead to? |
gluconeogenesis by proteolysis => thin skin
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Define conn's syndrome
What test will make it worse? |
high aldosterone tumor
Captopril test makes it worse |
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What is Addison's disease?
What does this lead to? |
Autoimmune destruction of adrenal cortex. Leads to ⇧ACTH and hyperpigmentation.
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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 |
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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 |
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Nelson's syndrome
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hyperpigmentation after adrenectomy and visual problems
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If low-dose dexamethasone test suppresses, what does that tell you?
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Patient is either depressed, obese, or it's a normal variant
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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) |
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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) |
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what are the survival hormones?
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cortisol: permissive under stress
TSH: permissive under normal |
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What does epinephrine do?
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gluconeogenesis, glycogenolysis
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What does erythropoetin do?
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makes RBC's
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What does gastrin do?
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stimulates parietal cells => IF, H+
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What does growth hormone do?
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growth, sends somatomedin to growth plates, gluconeogenesis by proteolysis
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What is pygmie?
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no somatomedin receptors
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What is achondroplasia (Laron Dwarf)?
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abnormal FGF receptors in extremities
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What is midget?
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decreased somatomedin receptor sensitivity
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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. |
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What is gigantism?
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childhood form of acromegally
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What does GIP do?
What does it lead to? |
Enhance insulin action responsable for post prandial hypoglycemia
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What does glucagon do?
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Gluconeogenesis, glycogenolysis, lipolysis, ketogenesis
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what does insulin do?
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pushes glucose into cells
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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
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What is type II Diabetes Mellitus?
presentation neck |
Insulin receptor insensitivity (high insulin)
Hyper osmolar non-etotic coma (HONK) Acanthosis nigricans |
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How does DKA present?
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kaussmal respirations, fruity breath (acetone), altered mental status
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Treatment for DKA?
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Insulin, NS, KCl, D5 1/2 NS
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What is dawn phenomenon? Tx
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morning hyperglycemia due to GH
Tx: increase pm insulin |
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What is somogyi effect?
Tx: |
morning hyperglycemia due to evening hypoglycemia.
Tx: decrease pm insulin |
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What is factitious hypoglycemia?
what are the insulin and c-peptide levels |
insulin injection (increase insulin, decrease c-peptide)
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What is insulinoma?
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tumor (increase insulin, increase c-peptide)
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What is erythrasma?
test tx: |
rash in skin folds
Test: Coral red under wood's lamp Tx: erythromycin |
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What is syndrome X = metabolic syndrome? tx:
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"Pre DM" => HTN, dyslipidemia, hyperinsulinemia, acanthosis nigrans
tx: metformin |
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What are the foot ulcer risk factors?
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DM/ Poor Glycemic control (HbA1c>7)
Smoker Bony abnormalities Previous ulcers |
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What are the 5 conditions causes weight gain?
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obesity
hypothyroidism depression cushing's anasarca |
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What does motilin do?
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stimulates segmentation which is primary peristalsis and migrating motor coplex (MMC)
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What does PTH do?
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Simulates osteoblast to activate osteoclast (chews up bone)
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What does vitamin D do?
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Help in calcium reabsorption from the GI tract (builds bone)
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what does the parathyroid chief cells secrete?
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PTH
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What do stomach chief cells secrete?
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pepsin
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what is the difference between Norepinephrine and epinephrine
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norepinephrine is a neurotransmitter and epinephrine is a hormone
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What diagnosis has primary hyperparathyroidism?
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parathyroid adenoma
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What diagnosis has secondary hyperparathyroidism?
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renal failure
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What is familial hypocalciuria hypercalcemia?
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decrease calcium excretion
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What disease process present when both serum calcium and PO⁴ are decreased?
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Vitamin D deficiency
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What type of problem is there if serum calcium and PO⁴ change in opposite directions?
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PTH problem (secondary)
high Ca => hyperPTH low Ca => hypoPTH |
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What is the most common cause of primary hypoparathyroidism?
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thyroidectomy
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what is pseudohypoparathyroidism?
what is decreased? |
bad PTH receptor on the kidney
decreased urinary cAMP |
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What is pseudopseudohypoparathyroidism?
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G-protein defect, no Ca₂⁺ problem
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What is hungry bone syndrome?
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Remove PTH and the bone sucks in Ca₂⁺
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What does secretin do?
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Secretion of bicarbonate, inhibits gastrin, and tighten pyloric sphincter
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What does somatostatin do?
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Inhibits secretin, motilin, CCK
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What do T₃ and T₄ do?
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growth and differentiation
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What disease has exophthalmos?
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Grave's disease
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What disease has enophthalmos?
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Horner's, Marfan's
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What does oxytocin do?
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milk ejection, baby ejection
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What does PRL do?
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milk production
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What are the 5 hyperthyroid diseases?
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Grave's
DeQuervain's Silent thyroiditis Plummer's Jod-basedow |
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What do you see in Grave's disease?
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Exopthalmos, pretibial myxedema, anti-TSH receptor antibodies
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What do you see in DeQuervain's disease?
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viral origin, painful jaw, hypo and hyperthyroid symptoms
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What do you see in silent thyroiditis ?
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post-partum patiens
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What would you see in Plummer's disease?
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patiens with benign adenoma and or patiens over 50 years old
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What is Jod-basedow disease?
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transient hyperthyroidism due to increased Iodine
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What are the 5 hypothyroid diseases?
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Hashimoto's
Reidel's struma Cretinism Euthyroid sick syndrome wolff-chaikoff |
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Hashimoto's antibodies
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antimicrosomal Ab =TPO Ab
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What is Reidel's struma?
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Woody connective tissue in the neck. Death due to suffocation. Rule out cancer
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What is Cretinism?
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mom and baby are hypothyroid. Features in the whrong place. Will have dietary problems.
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What is Euthyroid sick syndrome?
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low T₃ syndrome. Decrease convertion of T4 to T3
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What is Wolff-Chaikoff?
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transient hypothyroidism
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What is Plummer's syndrome?
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Hyperthyroid adenoma
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What is plummer-vinson syndrome?
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esophageal webs
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What does testosterone do?
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Makes external male genitalia
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What does mullerian Inhibiting factor (MIF) do?
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Inhibits formation of female internal structures
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What does thyroid peroxidase (TPO) and thymosin do?
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Help T cells mature
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what does vosoactitive interstitinal peptide (VIP) do?
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inhibit secretin, motilin, CCK. Opens sphincters.
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How does a VIPoma present?
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Watery diarrhea
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How does a SSoma present?
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Constipation
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What are the hormones with disulfide bonds?
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"PIGI"
Prolactin Inhibin Growth hormone Insulin |
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Which hormones have the same α subunits?
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LH, FSH
TSH β-HCG |
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Which hormones produce acidophils?
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"GAP"
GH PRL |
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What hormones produce basophils
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"B FLAT"
FSH LH ACTH TSH |
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Treatment strategy for type l DM
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low-sugar diet, insulin replacement.
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Treatment strategy for type lI DM
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dietary modification and exercise for weight loss; oral
hypoglycem ics and insulin replacement |
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What is the mechanism of action of insuline?
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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. |
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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. |
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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) |
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What is the mechanism of Sulfonylureas?
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Close K+ channel in the pancreatic beta cell membrane , so cell depolarizes
--> triggering of insulin release via increase Ca2+ influx. |
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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. |
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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. |
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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 |
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What are the adverse effect of Sulfonylureas?
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First generation : disulfiram like effects.
Second generation : Less side effects: hypoglycemia GI disturbances, muscle weakness, mental confusion |
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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 |
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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. |
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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 |
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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. |
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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. |
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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 |
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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. |
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What is the indication for Oxytosin?
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Induces labor; control uterine hemorrhage
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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 |
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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. |
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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 |
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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. |
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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. |