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291 Cards in this Set
- Front
- Back
|
50-year-old man complains of
diarrhea. On physical exam, his face is plethoric and a heart murmur is detected. |
Carcinoid syndrome.
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Woman of short stature presents
with shortened 4th and 5th metacarpals. |
Albright’s hereditary
osteodystrophy, or pseudohypoparathyroidism. |
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Surreptitious insulin injection.
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Nondiabetic patient presents
with hypoglycemia but low levels of C peptide. |
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Patient's MRI shows filling of
sella tursica with cerebrospinal fluid. What is the most likely clinical presentation? |
Normal. Residual pituitary tissue is functional and can compensate (empty sella syndrome).
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empty sella syndrome
|
sella tursica with cerebrospina
fluid. Residual pituitary tissue is functional and can compensate |
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Adrenal cortex and medulla
derivation |
Cortex (from mesoderm)
Medulla (from neural crest) |
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what controls the adrenal medulla
|
Preganglionic
sympathetic fibers |
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cell type in the adrenal medulla
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Chromaffin cells
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where are Chromaffin cells
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adrenal medulla
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Adrenal gland
drainage |
Left adrenal → left adrenal vein → left renal vein → IVC.
Right adrenal → right adrenal vein → IVC. |
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Posterior pituitary aka
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neurohypophysis
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neurohypophysis aka
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Posterior pituitary
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Posterior pituitary products
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vasopressin and oxytocin, made in the hypothalamus and
shipped to pituitary. |
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Anterior pituitary products
|
FLAT GiMP:
FSH LH ACTH TSH GH MSH (melanotropin) Prolactin |
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pituitary derivation
|
Posterior pituitary (neurohypophysis) → Derived from neuroectoderm.
Anterior pituitary (adenohypophysis) → Derived from oral ectoderm. |
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Anterior pituitary aka
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adenohypophysis
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adenohypophysis aka
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Anterior pituitary
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staining of ant pit hormones cells
|
Acidophils––GH, prolactin.
B-Flat: Basophils––FSH, LH, ACTH, TSH |
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Pituitary gland
and different subunits of hormones |
α subunit––common subunit to TSH, LH, FSH, and hCG.
β subunit––determines hormone specificity. |
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Pro-opiomelanocortin
|
POMC can be cleaved enzymatically into the following peptides:
# adrenocorticotropic hormone (ACTH) and β-Lipotropin in the anterior pituitary gland α-MSH and β-endorphin in the intermediate lobe |
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Endocrine pancreas cell types and products and locations
|
α = glucagon (peripheral);
β = insulin (central); δ = somatostatin (interspersed). |
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Endocrine pancreas where are the most δ endocrine cells
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in tail of pancreas
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Islets arise from
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pancreatic buds.
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regulation of Prolactin and implications
|
Prolactin ↑ dopamine synthesis and secretion from the hypothalamus. Dopamine
subsequently inhibits prolactin secretion. Dopamine agonists (e.g., bromocriptine therefore inhibit prolactin secretion, whereas dopamine antagonists (e.g., most antipsychotics) stimulate prolactin secretion. |
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Prolactin effects in females
|
prolactin inhibits GnRH
synthesis and release, which inhibits ovulation. Amenorrhea is commonly seen in prolactinomas. |
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Hypothalamic-pituitary hormone regulation
from hypo and what they do |
TRH—→ ↑ TSH, prolactin
Dopamine— → ↓ prolactin CRH— → ↑ ACTH GHRH—→ ↑ GH Somatostatin— → ↓ GH, TSH GnRH— → ↑ FSH, LH |
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Congenital bilateral adrenal
hyperplasias 17 α-hydroxylase deficiency labs |
↓ sex hormones, ↓ cortisol, ↑ mineralocorticoids.
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Congenital bilateral adrenal
hyperplasias 21 β-hydroxylase deficiency labs |
↓ cortisol (increased ACTH), ↓ mineralocorticoids,
↑ sex hormones. |
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Congenital bilateral adrenal
hyperplasias 21 β-hydroxylase deficiency clinial |
Cx = masculinization, female pseudohermaphroditism, HYPOtension, hyponatremia,
hyperkalemia, ↑ plasma renin activity, and volume depletion. Salt wasting can lead to hypovolemic shock in the newborn. |
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Congenital bilateral adrenal
hyperplasias 17 α-hydroxylase deficiency clinical |
Cx = HYPERtension,
hypokalemia; phenotypically female but no maturation. |
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Congenital bilateral adrenal
hyperplasias 11 β-hydroxylase deficiency labs |
↓ cortisol, ↓ aldosterone and corticosterone, ↑ sex hormones.
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Congenital bilateral adrenal
hyperplasias 11 β-hydroxylase deficiency clinical |
Cx = masculinization, HYPERtension (11-deoxycorticosterone acts as a weak mineralocorticoid).
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Congenital bilateral adrenal
hyperplasias Most common form |
21 β-hydroxylase deficiency
|
|
|
masculinization, female pseudohermaphroditism, HYPOtension, hyponatremia,
hyperkalemia, ↑ plasma renin activity, and volume depletion. Salt wasting can lead to hypovolemic shock in the newborn. |
21 β-hydroxylase deficiency
|
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PTH
Source |
Chief cells of parathyroid.
|
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PTH
Functions |
1. ↑ bone resorption of calcium and phosphate
2. ↑ kidney reabsorption of calcium in dct 3. ↓ kidney reabsorption of phosphate 4. ↑ 1,25-(OH)2 vitamin D (cholecalciferol) production by stimulating kidney 1 -hydroxylase |
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PTH
Regulation |
↓ in free serum Ca2+ ↑ PTH secretion.
|
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PTH
effect on ions |
PTH ↑ serum Ca2+, ↓ serum
(PO )3–, ↑ urine (PO )3–. |
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PTH
effect on bones |
PTH stimulates both
osteoclasts and osteoblasts. |
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If you do not get vitamin D, you get
|
rickets (kids) or
osteomalacia (adults). |
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24,25-(OH)2 vitamin D is
|
an inactive form of vitamin D.
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Vitamin D
Source/process |
Vitamin D3 from sun exposure in skin. D2 from plants. Both converted to 25-OH vitamin D in liver and to 1,25-(OH)2 vitamin D (active form) in kidney.
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Vitamin D
Function |
1. ↑ absorption of dietary calcium
2. ↑ absorption of dietary phosphate 3. ↑ bone resorption of Ca2+ and (PO4)3– |
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Vitamin D
Regulation |
--↑ PTH causes ↑ 1,25-(OH)2 production.
--↓ [Ca2+] causes ↑ 1,25-(OH)2 production. --↓ phosphate causes ↑ 1,25-(OH)2 produced --1,25-(OH)2 vitamin D feedback inhibits its own production. |
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-Calcium
-phosphate, -alkaline phosphatase levels Hyperparathyroidism |
↑
↓ ↑ |
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|
-Calcium
-phosphate, -alkaline phosphatase levels Paget’s disease of bone |
N/↑
N ↑↑↑ |
|
|
-Calcium
-phosphate, -alkaline phosphatase levels Vitamin D intoxication |
↑
↑ N/↑ |
|
|
-Calcium
-phosphate, -alkaline phosphatase levels Osteoporosis |
N
N N |
|
|
-Calcium
-phosphate, -alkaline phosphatase levels Renal insufficiency |
↓
↑ N |
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Calcitonin
Source |
Parafollicular cells (C cells) of thyroid.
|
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Calcitonin
Function |
↓ bone resorption of calcium.
Calcitonin opposes actions of PTH. It is probably not important in normal calcium homeostasis. |
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Calcitonin
Regulation |
↑ serum Ca causes calcitonin secretion.
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Steroid/thyroid hormones
names |
PET CAT:
Progesterone Estrogen Testosterone Cortisol Aldosterone Thyroxine and T3 |
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effects of changing levels of SHBG
|
↑ levels of sex hormone–binding globulin
(SHBG) lower free testosterone → gynecomastia. ↓ SHBG raises free testosterone → hirsutism. |
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Steroid hormones circulation and mech
|
Steroid hormones are lipophilic and relatively insoluble in plasma; therefore, they must
circulatebound to specific binding globulins, which ↑ solubility and allows for ↑ delivery of steroid to the target organ |
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Thyroid hormones
Source |
Follicles of thyroid. Most T formed in blood.
|
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Thyroid hormones
Function |
T3 functions––4 B’s:
Brain maturation Bone growth Beta-adrenergic effects BMR ↑ |
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Thyroid hormones
Regulation |
TRH (hypothalamus) stimulates TSH (pituitary), which stimulates follicular cells.
Negative feedback by T3 to anterior pituitary ↓ sensitivity to TRH. |
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|
Thyroxine-binding globulin
role |
(TBG) binds most T3/T4 in
blood; |
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|
Thyroxine-binding globulin
wrt activity |
Thyroxine-binding globulin
(TBG) binds most T3/T4 in blood; only free hormone is active. |
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things that affect Thyroxine-binding globulin
|
↑ TBG in pregnancy OCP or hormone replacement
↓ TBG in hepatic failure, steroids or nephrotic syndrome |
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TSI
|
TSI, like TSH, stimulates follicular cells (Graves’ disease).
|
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Insulin-dependent organs and mech
|
Skeletal muscle and adipose tissue depend on insulin for ↑ glucose uptake (GLUT-4).
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Insulin-independent organs and mech
|
Brain and RBCs take up glucose independent of insulin levels (GLUT-1).
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Cortisol
Source |
Adrenal fasciculata
|
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Cortisol
Functions |
1. Anti-inflammatory
2. ↑ gluconeogenesis, lipolysis, proteolysis 3. ↓ immune function 4. Maintains blood pressure 5. ↓ bone formation |
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Cortisol
Regulation |
CRH (hypothalamus) stimulates ACTH release (pituitary) causing cortisol production in
adrenal fasciculata. |
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Cortisol
wrt prolonged secretion |
Chronic stress induces
prolonged secretion. |
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Cortisol
binding |
Bound to corticosteroid binding
globulin (CBG). |
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Cushing’s syndrome
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↑ cortisol due to a variety of causes.
|
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Cushing’s disease
|
(1° pituitary adenoma); ↑
ACTH |
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(1° pituitary adenoma); ↑
ACTH |
Cushing’s disease
|
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↑ cortisol due to a variety of causes.
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Cushing’s syndrome
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causes of Cushing’s syndrome
|
1. Cushing’s disease (1° pituitary adenoma); ↑
ACTH 2. 1° adrenal (hyperplasia/neoplasia); ↓ ACTH (see Color Image 68) 3. Ectopic ACTH production (e.g., small cell lung cancer); ↑ ACTH 4. Iatrogenic (e.g., chronic steroids); ↓ ACTH |
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Cushing’s syndrome
clinical findings |
The clinical picture includes hypertension, weight
gain, moon facies, truncal obesity, buffalo hump, hyperglycemia (insulin resistance), skin changes (thinning, striae), osteoporosis, amenorrhea, and immune suppression |
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|
Dexamethasone suppression
test: |
Healthy––↓ cortisol after low
dose. pituitary ACTH-producing tumor ↑ cortisol after low dose; ↓ cortisol after high dose. scc of lung and or Cortisone -producing tumor––↑ cortisol after low and high dose. |
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|
Cushing’s syndrome test
|
Dexamethasone suppression
test: |
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Hyperaldosteronism
types |
Primary (Conn’s syndrome)
Secondary |
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Conn’s syndrome aka
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Primary Hyperaldosteronism
|
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Conn’s syndrome cause and effects
|
Caused by an aldosterone secreting tumor, resulting in hypertension, hypokalemia, metabolic alkalosis, and low plasma renin.
|
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Conn’s syndrome
Tx |
Treatment includes
spironolactone, a K+-sparing diuretic that works by acting as an aldosterone antagonist. |
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Secondary Hyperaldosteronism
causes and effects |
Due to renal artery stenosis, chronic renal failure, CHF, cirrhosis, or nephrotic syndrome. Kidney perception of low intravascular volume results in an overactive renin-angiotensin system. Therefore it is associated with high plasma renin.
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Hyperaldosteronism
which type has high renin |
Secondary
|
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Addison’s disease what is it
|
1° deficiency of aldosterone and cortisol due to adrenal atroph
|
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Addison’s disease
clinical findings |
hypotension (hyponatremic volume contraction)
and skin hyperpigmentation -Characterized by Adrenal Atrophy and Absence of hormone production; -involves All 3 cortical divisions. |
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|
Addison’s disease vs secondary
|
Distinguish from 2° insufficiency, which has no skin hyperpigmentation (↓ pituitary ACTH production).
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mech of hyperpigmentation in Addison's
|
due to MSH, a by-product of ↑ ACTH production from POMC
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Addison’s disease
what type of hypotension |
hyponatremic volume contraction
|
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The most common tumor of the adrenal medulla in
adults. |
Pheochromocytoma
|
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The most common tumor of the adrenal medulla in children
|
Neuroblastoma
|
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Neuroblastoma how common and where
|
The most common tumor of the adrenal medulla
in children, but it can occur anywhere along the sympathetic chain. |
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Pheochromocytomas may be
associated with |
neurofibromatosis,
MEN types II and III. |
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Pheochromocytoma
vs Neuroblastoma wrt urine |
Pheochromocytoma --VMA in urine.
Neuroblastoma --HVA in urine |
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VMA in urine.
|
Pheochromocytoma
|
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HVA in urine
|
Neuroblastoma
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Pheochromocytoma
clinical findings |
EPISODIC hyperadrenergic symptoms (5 P’s + anxiety):
Pressure (elevated blood pressure) Pain (headache) Perspiration (tachycardia) Palpitations Pallor |
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|
Neuroblastoma
clinical findings |
often vague and may include fatigue, loss of appetite, and fever
Less likely to develop hypertension. |
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Pheochromocytoma
derivation |
Derived from chromaffin cells (arise from neural crest)
|
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Postpartum hypopituitarism aka
|
Sheehan's syndrome
|
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Sheehan's syndrome aka
|
Postpartum hypopituitarism
|
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Sheehan's syndrome
mech |
infarction of the pituitary gland following severe bleeding and hypoperfusion during delivery.
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Sheehan's syndrome
clinical findings |
May cause fatigue, anorexia,
poor lactation, and loss of pubic and axillary hair. |
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Pheochromocytoma
Tx |
α-antagonists, especially phenoxybenzamine, a nonselective, irreversible α-blocker.
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Pheochromocytoma
mnemonic |
Rule of 10’s:
10% malignant 10% bilateral 10% extra-adrenal 10% calcify 10% kids 10% familial |
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Pheochromocytoma
Most of these tumors secrete |
Most of these tumors secrete epinephrine, NE, and dopamine.
|
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Pheochromocytoma
lab findings |
Urinary VMA levels and plasma catecholamines are elevated.
|
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MEN type I aka
|
Wermer’s syndrome
|
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Wermer’s syndrome aka
|
MEN type I aka
|
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MEN type II aka
|
Sipple’s syndrome
|
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Sipple’s syndrome aka
|
MEN type II
|
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MEN type III aka
|
formerly MEN IIb
|
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formerly MEN IIb
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MEN type III
|
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Multiple endocrine neoplasias (MEN)
inheritance |
All MEN syndromes have
autosomal-dominant inheritance. |
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Multiple endocrine neoplasias (MEN)
specific gene |
Associated with ret gene in
MEN types II and III. |
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MEN type I
involvement |
MEN I = 3 “P” organs
(Pancreas, Pituitary, and Parathyroid). (e.g., Zollinger-Ellison syndrome, insulinomas, VIPomas), parathyroid tumors, pituitary tumors (prolactinoma). |
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MEN type I
classic presentation |
Presents with kidney stones and
stomach ulcers. |
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(e.g., Zollinger-Ellison syndrome, insulinomas,
VIPomas), parathyroid, and pituitary tumors (prolactinoma). |
MEN type I (Wermer’s syndrome)
|
|
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MEN type II
involvement |
medullary carcinoma of the thyroid, pheochromocytoma,
parathyroid tumor. |
|
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medullary carcinoma of the thyroid, pheochromocytoma,
parathyroid tumor. |
MEN type II (Sipple’s syndrome)
|
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MEN type III
involvement |
MEN type III
medullary carcinoma of the thyroid, pheochromocytoma, and oral and intestinal ganglioneuromatosis (mucosal neuromas). |
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Hypothyroidism
findings |
Cold intolerance, hypoactivity, weight gain, fatigue,
lethargy, ↓ appetite, constipation, weakness, ↓ reflexes, myxedema (facial/periorbital), dry, cool skin, and coarse, brittle hair. |
|
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Hyperthyroidism
findings |
Heat intolerance, hyperactivity, weight loss, chest pain/palpitations, arrhythmias, diarrhea, ↑
reflexes, warm, moist skin, and fine hair. |
|
|
Riedel’s thyroiditis
|
thyroid replaced by fibrous tissue
(hypothyroid). |
|
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thyroid replaced by fibrous tissue
(hypothyroid). |
Riedel’s thyroiditis
|
|
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Graves’ disease
findings |
Hyperthyroid
Ophthalmopathy (proptosis, EOM swelling), pretibial myxedema, diffuse goiter. |
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Thyroid storm
findings |
Underlying Graves' disease with a stress-induced catecholamine surge leading to death
by arrhythmia. |
|
|
Underlying Graves' disease with a stress-induced catecholamine surge leading to death
by arrhythmia. |
Thyroid storm
|
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Graves’ disease Often
presents during |
stress (e.g., childbirth)
|
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Hashimoto’s thyroiditis
|
Autoimmune disorder resulting in hypothyroidism (can have thyrotoxicosis during follicular rupture).
|
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Autoimmune disorder resulting in hypothyroidism (can have thyrotoxicosis during follicular rupture).
|
Hashimoto’s thyroiditis
|
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Hashimoto’s thyroiditis
course and findings |
Slow course; moderately enlarged, nontender thyroid.
|
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Hashimoto’s thyroiditis
lab findings |
Lymphocytic infiltrate with germinal centers. Antimicrosomal and antithyroglobulin
antibodies. Hurthle cells. |
|
|
Lymphocytic infiltrate with germinal centers.
Antimicrosomal Ab's |
Hashimoto’s thyroiditis
|
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Hurthle cells.
|
Hashimoto’s thyroiditis
|
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Subacute thyroiditis aka
|
de Quervain’s)
|
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de Quervain’s aka
|
Subacute thyroiditis
|
|
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Subacute thyroiditis
(de Quervain’s) description |
Self-limited hypothyroidism often following a flulike illness. May be hyperthyroid early in course.
|
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|
Self-limited hypothyroidism often following a flulike illness
|
Subacute thyroiditis
(de Quervain’s) |
|
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Subacute thyroiditis
(de Quervain’s) labs |
Elevated ESR
|
|
|
Subacute thyroiditis
(de Quervain’s) clinical findings |
hypothyroidism
jaw pain, early inflammation, and very tender thyroid gland. |
|
|
Toxic multinodular goiter
mechanism |
Iodine deprivation followed by iodine restoration. Causes release of T3 and T4.
|
|
|
Toxic multinodular goiter
wrt cancer |
Nodules
are not malignant. |
|
|
Iodine deprivation followed by iodine restoration. Causes release of T3 and T4.
|
Toxic multinodular goiter
|
|
|
Jod-Basedow phenomenon
|
thyrotoxicosis if a patient with endemic goiter moves to
iodine-replete area. |
|
|
thyrotoxicosis if a patient with endemic goiter moves to
iodine-replete area. |
Jod-Basedow phenomenon
|
|
|
Wolff-Chaikoff effect
|
hypothyroidism caused by ingestion of a large amount of iodine.[1]
|
|
|
hypothyroidism caused by ingestion of a large amount of iodine
|
Wolff-Chaikoff effect
|
|
|
Thyroid cancer
most common |
Papillary carcinoma
|
|
|
Thyroid cancer
describe Papillary carcinoma |
most common,
excellent prognosis, “ground-glass” nuclei Orphan Annie), psammoma bodies. Increased risk with childhood irradiation. |
|
|
Thyroid cancer
Orphan Annie |
Papillary carcinoma
|
|
|
Thyroid cancer
psammoma bodies |
Papillary carcinoma
|
|
|
Thyroid cancer
Follicular carcinoma |
good prognosis, uniform follicles.
|
|
|
Thyroid cancer
good prognosis, uniform follicles. |
Follicular carcinoma
|
|
|
Thyroid cancer
Medullary carcinoma |
from parafollicular “C cells”; produces calcitonin, sheets of cells in amyloid stroma. MEN types II and III.
|
|
|
Thyroid cancer
from parafollicular “C cells” |
Medullary carcinoma
|
|
|
Thyroid cancer
produces calcitonin |
Medullary carcinoma
|
|
|
Thyroid cancer
sheets of cells in amyloid stroma |
Medullary carcinoma
|
|
|
Thyroid cancer
MEN types II and III. |
Medullary carcinoma
|
|
|
Thyroid cancer
Undifferentiated/anaplastic |
––older patients,
very poor prognosis. |
|
|
Thyroid cancer
older patients, very poor prognosis. |
Undifferentiated/anaplastic
|
|
|
Thyroid cancer
Lymphoma |
associated with Hashimoto's thyroiditis.
|
|
|
Thyroid cancer
associated with Hashimoto's thyroiditis. |
Lymphoma
|
|
|
Cretinism
endemic |
Endemic cretinism occurs wherever endemic goiter is prevalent (lack of dietary iodine)
|
|
|
Cretinism
sporadic |
defect in T4 formation or
developmental failure in thyroid formation. |
|
|
Cretinism
findings |
Findings: pot-bellied, pale, puffy-faced child with
protruding umbilicus and protuberant tongue. |
|
|
pot-bellied, pale, puffy-faced child with protruding umbilicus and protuberant tongue.
|
Cretinism
|
|
|
Cretinism
where still common |
china
|
|
|
Acromegaly
clinical and labfindings |
Excess GH in adults. Findings: large tongue with deep furrows, deep voice, large hands and feet, coarse facial features, impaired glucose tolerance
(insulin resistance). |
|
|
↑ GH is normal in
|
stress,
exercise, and hypoglycemia. |
|
|
↑ GH in children →
and Tx |
gigantism. Treat medically with octreotide.
|
|
|
Acromegaly
test |
Test with oral glucose tolerance
test. GH levels not suppressed below 1 μg/L means acromegaly. |
|
|
Primary Hyperparathyroidism
cause |
Usually an adenoma
|
|
|
Primary Hyperparathyroidism
clinical and lab findings |
“Stones, bones, and groans.”
Hypercalcemia, hypercalciuria (renal stones), hypophosphatemia, ↑ PTH, ↑ cAMP in urine. Often asymptomatic, or may present with weakness and constipation (“groans”). |
|
|
secondary Hyperparathyroidism
mech |
2° hyperplasia due to ↓ serum Ca2+, most often in
chronic renal disease. |
|
|
secondary Hyperparathyroidism
findings |
Renal osteodystrophy
Hypocalcemia, hyperphosphatemia, ↑ PTH. |
|
|
Renal osteodystrophy
|
bone lesions due to 2˚ hyperparathyroidism due in turn to renal disease.
|
|
|
bone lesions due to 2˚ hyperparathyroidism due in turn to renal disease.
|
Renal osteodystrophy
|
|
|
Hypoparathyroidism
causes |
Due to accidental surgical
excision (thyroid surgery) or DiGeorge syndrome. |
|
|
Due to accidental surgical
excision or DiGeorge syndrome. |
Hypoparathyroidism
|
|
|
Hypoparathyroidism
findings |
Hypocalcemia, tetany
Chvostek’s sign– Trousseau sign of latent tetany- |
|
|
Chvostek’s sign
|
tap facial nerve → contraction of
facial muscles. |
|
|
tap facial nerve → contraction of
facial muscles. |
Chvostek’s sign
|
|
|
Trousseau’s sign (not of malignancy)
|
––occlusion of brachial artery with
BP cuff → carpal spasm. |
|
|
––occlusion of brachial artery with
BP cuff → carpal spasm. |
The Trousseau sign of latent tetany
|
|
|
The Trousseau sign (not of latent tetany)
|
a medical sign found in certain cancers that is associated with hypercoagulability. esp specially adenocarcinomas of the pancreas and lung,
|
|
|
sign found in certain cancers associated with hpercoagulability.
|
Trousseau sign of malignancy
|
|
|
Pseudohypoparathyroidism
genetics, mech, lab, clinical |
autosomal-dominant kidney
unresponsiveness to PTH. Hypocalcemia, shortened 4th/5th digits, short stature. |
|
|
Pseudohypoparathyroidism
inheritance |
autosomal-dominant
|
|
|
autosomal-dominant kidney
unresponsiveness to PTH. |
Pseudohypoparathyroidism
|
|
|
Hypocalcemia, shortened
4th/5th digits, short stature. |
Pseudohypoparathyroidism
|
|
|
Hypercalcemia
causes |
CHIMPANZEES.
Calcium ingestion (milk-alkali syndrome),Hyperparathyroid/thyroid, Iatrogenic (thiazides), Multiple myeloma, Paget’s, Addison’s, Neoplasms, Zollinger-Ellison, Excess vitamin D, Excess vitamin A, Sarcoidosis. |
|
|
Pituitary adenoma
most common type |
prolactinoma
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Pituitary adenoma
most common type and findings |
prolactinoma
ammenorrhea, galactorrhea, low libido, infertility. |
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Pituitary adenoma
Tx |
Bromocriptine (dopamine agonist) causes shrinkage.
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Bromocriptine (dopamine agonist) causes shrinkage.
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prolactinoma
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Diabetes mellitus
Acute manifestations (8) |
Polydipsia, polyuria, polyphagia, weight loss, DKA (type 1), hyperosmolar coma (type 2), unopposed secretion of GH and epinephrine (exacerbating hyperglycemia).
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Diabetes mellitus
chronic manifestations due to Nonenzymatic glycosylation: |
1. Small vessel disease (diffuse thickening of basement membrane) → retinopathy, glaucoma,
nephropathy 2. Large vessel atherosclerosis, CAD, peripheral vascular occlusive disease and gangrene, cerebrovascular disease |
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Diabetes mellitus
chronic manifestations due to Osmotic damage: |
1. Neuropathy (motor, sensory, and autonomic degeneration)
2. Cataracts (sorbitol accumulation) |
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Tests for DM
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Fasting serum glucose,
glucose tolerance test, HbA1c (measures long-term diabetic control). |
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DM and HLA
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Type 1 (HLA-DR3 and 4)
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IDDM aka
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Type 1––juvenile onset
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Type 1––juvenile onset aka
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IDDM
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NIDDM aka
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Type 2––adult onset
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Type 1 vs. type 2 diabetes mellitus
wrt Ketoacidosis |
Type 1––Common
Type 2––Rare |
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Type 1 vs. type 2 diabetes mellitus
wrt β-cell numbers in the islets |
Type 1––↓
Type 2––Variable |
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Type 1 vs. type 2 diabetes mellitus
wrt Serum insulin level |
Type 1––↓
Type 2––Variable |
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Type 1 vs. type 2 diabetes mellitus
wrt Classic symptoms of polyuria, polydipsia, thirst, weight loss |
Type 1–– Common
Type 2––Sometimes |
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Type 1 vs. type 2 diabetes mellitus
wrt 1° defect |
Type 1––Viral or immune destruction of β cells
Type 2––↑ resistance to insulin |
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Diabetic ketoacidosis
mech |
Usually due to ↑ insulin requirements from an ↑ in stress (e.g., infection). Excess fat breakdown and ↑
ketogenesis from the ↑ in free fatty acids, which are then made into ketone bodies. |
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Diabetic ketoacidosis
Signs/symptoms |
Kussmaul respirations, hyperthermia, nausea/vomiting, abdominal pain, psychosis/dementia, dehydration. Fruity breath odor (due to exhaled acetone).
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Diabetic ketoacidosis
Labs |
Hyperglycemia, ↑ H , ↓ HCO3 (anion gap metabolic acidosis),
↑ blood ketone levels, leukocytosis. Hyperkalemia, but depleted intracellular K+. |
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Diabetic ketoacidosis
Complications |
Life-threatening mucormycosis, Rhizopus infection, cerebral edema, cardiac arrhythmias,
heart failure. |
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Diabetic ketoacidosis
Treatment |
Fluids, insulin, and potassium; glucose if necessary to prevent hypoglycemia.
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Kussmaul respirations
what and cause |
(rapid/deep breathing)
The cause of Kussmaul breathing is respiratory compensation for a metabolic acidosis, most commonly occurring in diabetics in diabetic ketoacidosis. |
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Diabetes insipidus
clinical findings |
intensive thirst and polyuria together
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Diabetes insipidus
Diagnosis |
Water deprivation test––urine osmolality doesn’t ↑.
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Diabetes insipidus
lab Findings |
Urine specific gravity < 1.006; serum osmolality > 290 mOsm/L.
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Central Diabetes insipidus
Treatment |
Adequate fluid intake.
–intranasal desmopressin (ADH analog). |
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Central Diabetes insipidus
mech |
lack of ADH
(pituitary tumor, trauma, surgery, histiocytosis X) |
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Nephrogenic Diabetes insipidus
mech |
lack of renal response to ADH (hereditary or
2° to hypercalcemia, lithium, demeclocycline) |
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Nephrogenic Diabetes insipidus
Tx |
fluid intake
-hydrochlorothiazide, indomethacin, or amiloride. |
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SIADH
causes |
1. Ectopic ADH (small cell
lung cancer) 2. CNS disorders/head trauma 3. Pulmonary disease 4. Drugs (e.g., cyclophosphamide) |
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SIADH
labs |
1. Excessive water retention
2. Hyponatremia 3. Urine osmolarity > serum osmolarity |
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SIADH
complications |
Very low serum sodium levels can lead to seizures
(correct slowly). |
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SIADH
Tx |
Treat with demeclocycline or H2O restriction.
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Carcinoid syndrome
causes |
carcinoid tumors especially metastatic small bowel tumors, which secrete high levels of serotonin (5-HT).
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Carcinoid syndrome
wrt location and why |
Not seen if tumor is limited to
GI tract (5-HT undergoes first-pass metabolism in liver). |
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Carcinoid syndrome
symptoms |
Results in recurrent diarrhea, cutaneous flushing, asthmatic wheezing, and right-sided valvular disease.
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Most common tumor of
appendix. |
carcinoid tumors
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carcinoid tumor
derivation |
neuroendocrine cells (usually of the GI tract)
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Carcinoid syndrome
Dx |
↑ 5-HIAA in urine.
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↑ 5-HIAA in urine.
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Carcinoid syndrome
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Carcinoid syndrome
Tx |
octreotide.
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carcinoid tumor
mnemonic |
Rule of 1/3s:
1/3 metastasize 1/3 present with 2nd malignancy 1/3 multiple |
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Zollinger-Ellison syndrome
what, where, complications, associations |
Gastrin-secreting tumor of pancreas or duodenum. Causes recurrent ulcers. May be
associated with MEN type I. |
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Gastrin-secreting tumor of pancreas or duodenum
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Zollinger-Ellison syndrome
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Treatment strategy for type 1 DM–
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low-sugar diet, insulin replacement.
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Treatment strategy for type 2 DM
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dietary modification and exercise for weight loss;
oral hypoglycemics. |
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Sulfonylureas:
Names |
-ide
First generation: Tolbutamide Chlorpropamide Second generation: Glyburide Glimepiride Glipizide |
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Sulfonylureas:
Mech |
Close K+ channel in β-cell membrane, so cell depolarizes →
triggering of insulin release via ↑ Ca2+ influx. |
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Sulfonylureas:
Clinical use |
Stimulate release of endogenous insulin in type 2 DM.
useless in type 1 |
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Sulfonylureas:
Toxicity |
First generation:
disulfiram-like effects. Second generation: hypoglycemia. |
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Close K+ channel in β-cell membrane, so cell depolarizes →
triggering of insulin release via ↑ Ca2+ influx. |
Sulfonylureas:
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Insulin:
names and time frames |
Lispro (short-acting)
Insulin (short-acting) NPH (intermediate) Lente (long-acting) Ultralente (long-acting) |
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Insulin:
mech and action in different tissues |
Binds insulin receptor
(tyrosine kinase activity). Liver: ↑ glucose stored as glycogen. Muscle: ↑ glycogen and protein synthesis, K+ uptake. Fat: aids TG storage. |
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Insulin:
Clinical Use |
Type 1 DM. uncontrolable type 2
Also life-threatening hyperkalemia and stress-induced hyperglycemia. |
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Insulin:
Toxicity |
Hypoglycemia,
hypersensitivity reaction (very rare). |
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Biguanides
names |
Metformin
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Biguanides
mech |
Exact mechanism is unknown. Possibly ↓gluconeogenesis, ↑
glycolysis, ↓ serum glucose levels. |
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Biguanides
clinical use |
type 1 and 2
Used as oral hypoglycemic. Can be used in patients without islet function. |
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Biguanides
Toxicity |
lactic acidosis.
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DM drugs
lactic acidosis. |
Biguanides: (Metformin)
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Used as oral hypoglycemic.
Can be used in patients without islet function. |
Biguanides: (Metformin)
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Glitazones
names |
Pioglitazone
Rosiglitazone |
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Glitazones
mech |
↑ target cell response to
insulin. |
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Glitazones
clinical use |
monotherapy in type 2 DM or combined with other agents.
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Glitazones
toxicity |
Weight gain, edema.
Hepatotoxicity (troglitazone— no longer used). |
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Weight gain, edema.
Hepatotoxicity (troglitazone— no longer used). |
Glitazones
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α-glucosidase inhibitors:
names |
Acarbose
Miglitol |
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α-glucosidase inhibitors:
mech |
Inhibit intestinal brush
border α-glucosidases. Delayed sugar hydrolysis and glucose absorption lead to ↓ postprandial hyperglycemia. |
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α-glucosidase inhibitors:
clinical use |
Used as monotherapy in
type 2 DM in combination with other agents. |
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α-glucosidase inhibitors:
Toxicity |
GI disturbances.
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Inhibit intestinal brush
border α-glucosidases. Delayed sugar hydrolysis and glucose absorption lead to ↓ postprandial hyperglycemia. |
α-glucosidase inhibitors:
Acarbose Miglitol |
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Orlistat
Mechanism |
Alters fat metabolism by inhibiting pancreatic lipases.
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Orlistat
Clinical use |
ong-term obesity management (in conjunction with modified diet).
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Orlistat
Toxicity |
Steatorrhea, GI discomfort, reduced absorption of fat-soluble vitamins, headache.
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Sibutramine
Mechanism |
Sympathomimetic serotonin and norepinephrine reuptake inhibitor.
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Sibutramine
Clinical use |
Short-term and long-term obesity management.
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Sibutramine
Toxicity |
Hypertension and tachycardia.
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Sympathomimetic serotonin and norepinephrine reuptake inhibitor. for weight loss
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Sibutramine
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Alters fat metabolism by inhibiting pancreatic lipases.
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Orlistat
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Propylthiouracil, methimazole
Mechanism |
Inhibit organification and coupling of thyroid hormone synthesis. Propylthiouracil also
↓ peripheral conversion of T to T . |
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Propylthiouracil, methimazole
Clinical use |
Hyperthyroidism.
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Propylthiouracil, methimazole
Toxicity |
Skin rash, agranulocytosis (rare), aplastic anemia.
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Inhibit organification and coupling of thyroid hormone synthesis. ???????also
↓ peripheral conversion of T to T . |
Propylthiouracil, methimazole
Propylthiouracil |
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GH
Clinical use |
GH deficiency, Turner’s syndrome
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octreotide
Clinical use |
Acromegaly, carcinoid, gastrinoma, glucagonoma
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Oxytocin
Clinical use |
Stimulates labor,
uterine contractions, milk let-down; controls uterine hemorrhage |
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desmopressin
Clinical use |
Pituitary (central, not nephrogenic) DI
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octreotide aka
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Somatostatin
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Somatostatin drug
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octreotide
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ADH aka
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desmopressin
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desmopressin aka
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ADH
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Levothyroxine, triiodothyronine
Mechanism |
Thyroxine replacement.
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Levothyroxine, triiodothyronine
Clinical use |
Hypothyroidism, myxedema.
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Levothyroxine, triiodothyronine
Toxicity |
Tachycardia, heat intolerance, tremors.
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myxedema describe it
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the accumulation of increased amounts of hyaluronic acid and chondroitin sulfate in the dermis in both lesional and normal skin
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the accumulation of increased amounts of hyaluronic acid and chondroitin sulfate in the dermis in both lesional and normal skin
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myxedema
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Glucocorticoids
names |
Hydrocortisone,
prednisone, triamcinolone, dexamethasone, beclomethasone. |
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Glucocorticoids
Mechanism |
↓ the production of leukotrienes and prostaglandins by inhibiting phospholipase A2 and expression of COX-2.
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Glucocorticoids
Clinical use |
Addison’s disease, inflammation, immune suppression, asthma.
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