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140 Cards in this Set

  • Front
  • Back
Cortisol Function
Gluconeogenesis by proteolysis, thin skin
Epinephrine function
Gluconeogenesis and Glycogenolysis in liver/adrenal cortex
GH function
Gluconeogenesis by proteolysis in liver→ IGF-1 “somatomedin” to growh plates
GIP function
Enhances insulin action in pancrease→ post-prandial hypoglycemia
GIP syndromes
Dumping sndrome: seen after Bilroth II procedure
Dumping Syndrome Features
Increased osmotic load dumped into duodenum, causes osmotic diarrhea, can also cause postprandial (reactive) hypoglycemia. Insulin resistance over time (Type 2DM)
Motilin function
Stimulates primary peristalsis, MMC in duodenum
Secretin function
Secretion of bicarb, inhibits gastrin, tightens pyloric sphincter
Somatostatin function
Inhibits secretin, motilin, CCK
VIP function
Inhibits secretin, motilin, CCK
ADH stimulated by
Stress, high osmolarity
Diabetes insipidus –Nephrogenic Tx
THiazide diuretics (paradoxical effect)
DI- Central DI Tx
Serum Na<115 is what disease
SIADH (too much ADH)→ pee Na/retain H20
Causes of SIADH
Pain, Carbamezapine, Amphotericin B, Cancer, Increased ICP, Restrictive lung disease
Fluid restriction (Turn IV down) or Demecocylcine/Li (ADH antagonists)
Sx when Na<120
Seizures, arrhythmias (tx: 3% NS)
Psychogenic Polydipsia lab
Low plasma osmolarity, appropriate ADH levels
POMC (propiomelanocortin) is?
Opio (B-endorphin-feel no pain) Melano-MSH (dark sin), Cortin (ACTH)
Conn Syndrome Sx and Lab values
HTN, H/A, muscle weakness, Decreased Renin
Conn’s syndrome Test
24 hr urine Aldo on high salt diet
Conn’s syndrome Tx:
ACE-I (increase K+), Spironolactone (blocks Aldo), Adrenalectomy
Salt craving, Hyperpigmentation, Orthostatic Hypotension
Low Cortisol
Addison’s Disease Tx
Addisonian Crisis
Fever, change in mental status, ab pain, Orthostatic Hypotension (Tx: hydrocortisone)
Water-house Friderichsen syndrome Tx
Emergent Methylprednisolone
Purulent Fallopian Tubes to Adrenals, to liver
Adrenals (Waterhouse-Friderichsen-N.meningitidis), Liver (Fitz-Hugh-Curtis- N.gonorrhea)
Nelson’s syndrome
Pt w/ cushing had bilateral adrenalectomy, years later has hyperpgimentation+ visual problems d/t unsuppressed pituitary adenoma (Increased ACTH)
Adrenal tumor in Kids, high spontaneous regression rate, Ab mass, Dancing eyes “hypsarrhytmia”, Dancing feet “myoclonus”
Contraindicated in Pheochromocytoma
B-blocks (unopposed Alpha stimulation causes rapid Increase in BP)
Pre-op Pheochromocytoma Tx
14d Phenoxybenazmine+ Fluid Load (increase NA+ diet)
Operative Tx Pheochromocytoma
Phentolamine (blocks Alpha Nonspecific)→ adrenalectomy→ increase NE/Epi→ HTN crisis→ B1 blocker (everythigns blocked except B2)→ depending on IVF to keep BP up…
Insulin is stimulated by, inhibited by
Stimulated (hyperglycemia, Stress, B2 receptors), Decreased (alpha2 receptors)
DM Tx to slow progression of Nephropathy
DM type I genetics
Acanthosis Nigracans <50
<50=DM type II
Acanthosis Nigracans >50
>50= Stomach Ca
Dawn Phenomenon
3 am Increase glucose d/t GH (Tx: Increase PM insulin)
Somogy Effect
3 am decreased glucose→ 6 am Increased glucose (Tx: decrease pm insulin)
Factitious Hypoglycemia
d/t insulin injection (increase insulin, Decreased C-peptide)
Rash in skin folds, coral red Wood’s lamp, micrococcus infection
Erythrasma Tx
Syndrome X
Metabolic syndrome (Pre-DM=HTN, Dyslipidemia, Hyperinsulinemia)
Syndrome X Dx
Fasting glucose 111-125 AND Glucose challenge 140-200 mg/dl
Syndrome X Tx
Tight glycemic control will decrease risk of?
Retinopathy, nephropathy, neuropathy, Fetal abnormalities
What activities decrease Glucose in blood?
Alcohol, Exercise, Pregnancy, Delayed Gastric Emptying
How do you Diagnose DM?
Random glucose >200 w/ sx OR Fasting glucose>126 (w/ 1x repeat) OR Glucose Challenge (75g>200 @2 hrs)
What is the physiology of DM Retinopathy?
Weak capillary BM: leak plasma→ Retina. (Microaneursysms, Hard exudates (sharp demarcation), Dot-blot hemorrhages, Flame hemorrhages)
What do you see in Pre-Proliferative DM retinopathy?
Edema of Macula, Infarction of retina (hypoxia)→ soft exudates, “cotton-wool spots”
What do you see in PROLIFERATIVE DM retinopathy?
Neovascularization, Ruptures, Heal→ collagen pulls→ retinal Detatchment
HbA1c measures?
Glycemic control over past 3 months= RBC lifespan
What is a good glycmic control? When do you get a false positive?
<6%= good HbA1c. False+ w/ Hemolytic Anemia
What hormones have the same Alpha Subunits?
Short Acting insulin?
Lispro, Regular, Asparte
Intermediate acting insulin?
NPH, Lente
Long Acting Insulin?
Glargine, Ultralente
What are Weight Gain differentials?
Obesity, Hypothyrodism, Depression, Cushing’s, Anasarca
Diet modifications for Type 2 DM?
Low sat fats, and Exercise (weight loss upregulates insulin receptors)
Sulfonylureas, Alpha-glucosidase inhibitors, Biguanides,
1st generation sulfonylureas AE
Weight gain, Hypoglycemia* (Chlorpropramide- SIADH), Tolbutamide, Tolazamide
Glipizide, Glyburide (like 1st but inhibit gluconeogenesis and enhance peripheral glucose uptake)
Where is glyburide metabolized?
Sulfonylurea Overdose Treatment?
Dextrose, then Octreotide (inhibits insulin secretion)
Inhibits Gluconeogenesis. AE: reacts w/ IV dyes, severe metabolic acidosis
What are the Meds to tx DM type II
Thiazolidinediones: Incrase insulin sensitivity, check ALT/AST
Pancrease Delta cells and Duodenum. Goes nowhere has Paracrine function
Inhibits secretin, motilin, CCK
High insulin, Glucagon
Somatostainoma will cause?
Steatorrhea, gallstones and DM like sx
Duodenum. Goes to Pancrease and GB
Secretion of Bicarb, Inhibits: gastrin. Tightens pyloric sphincter. cAMP
Secretin is stimulated by?
Low pH
What stimulates CCK release, inhibits?
Simulated by Fat, Inhibited by High pH
Enhances insulin action⇒ post-prandial hypoglycemia
Low pH, glucose
High pH>2
Parathyroid Chief cells
Bone, kidney
Low Ca, high Phosphate
Parathryoid→ PTH. Stomach→ Pepsin
Both decreased
Calcium decreased, Phosphate Increased (vice versa in HyperPTH)
Activates Osteoclasts (needs Vit A and Mg)→ High Ca2+
In Proximal Tubule→ waste phosphoruous→ Low PO4. In Distal tubules→ Activates 1-Alpha Hydroxylase→ activate Vit D
GI (stimulates Ca-binding protein→ High PO4). Kidney DT
Cholecalciferol (D3)
Calcifediol (25-OH)VitD2 (from 1-Alpha hydroxylase activated by PTH)
Vitamin D in kidney?
Calcitriol (1,25-OH2) vit D
Primary Parathyroid Adenoma (MEN1,2), 2ndary Renal failure, Sarcoidosis
Increased PTH and Ca2+, Decreased Phosphate. SX: “Bones-osteoclasts, Groans- pancreatitis (gi upset,ulcers), Stones- kidney, stones, Moans- psychosis”
Subperiosteal thinning (erosion). MC- Medial side of 2nd and 3rd
Decrease Calcium (Furosemide, Calcitonin, Bisphophonates). Parathyroidectomy (Decrase Ca2+→ can cause Bells palsy)
Cant absorb/secrete→ Pseudohypo profile: Increased PTH and
Oral Ca2+ (decrease Phosphate to avoid metastatic calcifications)
Bad kidney PTH RECEPTOR (increased PTH, Decreased Ca, increased Phosphate)
Pseudo-hypo-parathyroidism presentation and clinical syndrome:
Sausage digits (short 3rd/5th digits), Albright’s Osteodystrophy,
G-protein defect→ no cAMP (Increased PTH, phosphate, normal calcium)
Familial Hypocalciuria Hypercalcemia:
Decreased Calcium excretion (urine Ca<200)
Oral/GI neuromas (MENIII)
Thryoglobulin: I-Tyr-MIT (or DIT) in colloid
Liver: T4→ T3, and when ur Sick T4→ rT3 (inactive storage when your sick)
Exopthalmos is seen in:
Graves, Histiocytosis X, Carvernous sinus thrombosis
Enopthalmos is seen in:
Exopthalmos, Pretibial (hard) myxedema, increased risk of Myasthenia graivs
Graves Disease TX
Radio-iodine ablation+ Prednisone (for eyes)
Subactue granulomatous Thyroidistis (viral Ix invades thyroid→ painful jaw)
Neutrophils, lymphocytes, histiocytes, multinucleated giant cells= Mixed cell infiltration
Increased ER, Tender/warm thyroid, Lid lag, Decreased Uptake
Dequervain’s Tx
Propanolol/PTU or Methimazole
. Post partum (Immune system attacks after pregnancy→ attacks
Benign “toxic” adenoma in old people→ increased radioactive
(+)= Hyperthyroid/Adenoma. Non= THyroiditis. Low= Folicular
Check free T4.
Iodine scan→ FNA (if cold)
5-HT, TSH, Nipple stimulation
Prolactin 1st> GH>FSH/LH (secondary amenorrhea, male impotence)>TSH (hypothyroid), ACTH
No somatomedin receptors
=Laron Dwarf: abnormal FGF receptors (extremeties only)
More OsteoCLASTIC activity> osteoblastic. Loss of bone matrix or osteoid
Loss of mineralization= soft bone
Decreased Osteoclast activity. Too much bone, Thick +Heavy bone. Oblierates BM. Bone is too thick and inflexible
Loss of Bone mass, bone matrix and mineralization is lost
Osteitis Deformans
=Paget’s Disease of bone. Increased Osteoclastic activity (increase bone breakage and bone building). Normal serum calcium at first, increased LAP
Paget’s Disease increased risk for? Genetics, Virus?
10% increase risk of Bone Cancer. Paramyxovirus. Increased P53, oncogene gain function
Paget’s disease Tx
Bisphophonates, +/- Calcitonin
Scarring of bone, occur in any inflammation of bone