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Endo-NBME Flashcards

1
Q

CF of Hypocalcemia ?

A

Peri-oral tingling
carpopedal spasms
muscle cramps
Tetany
Seizures

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2
Q

CF of Primary Hypoparathyroidism

A

Hypocalcemia
Hyperphosphatemia

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3
Q

Why do patients with Liver failure/ laceration suffer from Hypocalcemia post Tx ?

A

Citrate is usually metabolized in the liver.
Since liver isnnot as active, citrate is not metabolized and is bound to Free Ca, leading to hypocalcemia.

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4
Q

PTH effect on Calcium

A

1- Kidneys: increase calcium reabsorption, activation of 1,25-dihydroxyvitamin D,
2- leading to increase of Ca. absorption in Gut
3- and increase bone resorption, increasing calcium levels.

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5
Q

What is the physiologically active form of Calcium ?

A

Ionized calcium

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6
Q

Calcium binding to albumin is affected by ?

A

PH (increased PH like alkalosis, dissociates H+ from albumin, increasing albumin affinity to calcium–> leading to signs of hypocalcemia)

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7
Q

Clinical evaluation of hypercalcemia

A
  1. Repeat test, incleading corrected for albumin levels
  2. Check PTH
  3. if PTH is normal or High ( hypercalcemia is PTH dependant)
    4if PTH is supressed (Hypercalcemia is PTH in-dependant, chec other causes like PTHrP, 25,hydroxyvitamin d and 1,25-dihydroxy vitamin D.
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8
Q

Hypercalcemia of malignancy leads to

A

Severe Hypercalcemia > 14

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9
Q

Hyper calcemia bkg of Sarcoidosis

A

Hypercalcemia because of increased conversion of 25hydroxyviTD to 1,25-dihydroxyvitD

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10
Q

Effect of osteoporosis on Calcium levels

A

No increase

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11
Q

Effect of Calcium on Kindeys

A
  1. Vasoconstriction of afferent arterioles –> low eGFR –> Na and HCO3 retention at PCT.
  2. High Ca at Ca-sensing receptors in ascending Loop of henle –> inhibits Na/K/cl- and leads to hypovolemia –> release of RAA and aldosterone to try and increase Na as a result H excretion
  3. Inhibits ADH receptors in CT and inhibits water reabsorption.
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12
Q

CF of Milk alkali syndrome ?

A

1- hypovolemia, polyuria and increased thirst
2- Alkalosis (increased HCO3 retntion and H excretion)
3- Hypercalcemia

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13
Q

What is the effect of Hyperthyroidism on Calcium levels

A

Hypercalcemia and hypercalciuria.
Starts by direct osteolytic activity of Thyroids hormones on bones –> High Ca –> Inhibits PTH

Also inhibits conversion to active vit D, decr. Ca reabsorption for gut
and increase calcium excretion in kidneys.

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14
Q

What is silent Thiroiditis or postpartum thyroiditis ?

A

fprm of Hashimoto Thyroiditis
TPO positive
small non tender goiter
low t4, high TSH

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15
Q

CF of hypothyroidism

A

Anxiety
weight gain
normal apetite
bradycardia
cold intolerance
Constipation
decreased concentration and memory

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16
Q

Complications of hypothyroidism

A

hypercholesterolemia, hypertriglyceredemia
Hyponatremia
elevated transaminases
elevated ck, myopathy

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17
Q

CF of Thyroid storm or Thyrotoxicosis

A

1- Fever
2- Palpitations/ AF/ tachycardia
3- HTN
4- Lid lag

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18
Q

Neonatal Thyrotoxicosis ( on Background of Maternal Graves disease)

A

Transplacental Thyroid receptors antibodies.

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19
Q

Mangement of Graves Disease ?

A

Anti-thyroid meds
Radioactive Iodine
Thyroidectomy

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20
Q

Side Effects of Radioactive Iodine ?

A

worsen opthalmopathy by increasing TRAB.

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21
Q

What is a Euthyroid sick syndrome

A

aka low T3 syndrome

Normal T4 and TSH, low t3 due to decreased coversion of t4 to t3.

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22
Q

Management of thyrotoxicosis ?

A

1- Propranolol (symptom control)
2- PTU ( to decrease synthesis of TH)
3- Cortisol (stop conversion of T4 to t3)
4- Iodine solution ( to stop the release of thyroid hormones from gland).
5- Identify the stressor.

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23
Q

Effect of OCP or prhegnancy on thyroid hormone

A

Increases Thyroid binding globulins, more T4 are bound to TBG.
So thryroid will try to produce more to maintain a euthyroid stage.

Total T4 is increased
Free T4 is normal
TSH Normal

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24
Q

Medullary Cancer has high

A

Calcitonin

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25
Follicular Thyroid Cancer evaluation ?
Iodine scintigraphy: cold nodule Unable to diff. from Benig follicular adenoma on FNA Invasion of tumor capsule and bv on excision indicate its nature.
26
CF of Papillary thyroid cancer and management
Psammoma bodies Surgery resection and Iodine ablation post-op appropriate thyroxine supplementation, to prevent TSH release ( due to increased risk of recurrence).
27
SE of PTU and Methamizole and when to stop them
Agranulocytosis In cases of infection
28
MEN type 1
1. Pituitary adenoma 2. Primary Hyperparathyroidism 3. Pancreatic Cancer
29
What is Sheehan Syndrome ?
It is ischemic necrosis of the pituitary gland, due to hemorrhagic shock during birth
30
CF of Sheehan Syndrome ?
1. Low prolactin --> lack of lactation. 2. Secondary Adrenal insufficiency --> persistent hypotension, weight loss), no ACTH, no cortisol 3. Cental hypothyroidism, fatugue, brady 4. Hypogonadotropic hypogonadism ( ammenorrhea). low FSH and LH 5. decreased GH --> decreased lean body mass.
31
CF of hypopituitarism ?
Hypothyroidism (low TSH, low T4)--> signs Central adrenal insufficiency ( low ACTH and cortisol) --> hypoglycemia hypogonadotropic hypogonadism ( low LH, FSH and testosterone)--> decreased libido, erectile dysfunction. Normal aldosterone: not affected by ACTH mainly controlled by RAA).
32
Primary Adrenal Insufficiency AKA Addisons disease
Addisons failed to have cortisol and aldosterone. Low cortisol levels, high ACTH levels Low aldosterone: hyponatrema and hypokalemia. Confirmation: Cosyntropin (ACTH stimulation test) will lead to a minimal increase in cortisol.
33
How to differentiate PAI and Central adrenal insufficiency ?
hyperpigmentation and hyperkalemia seen in PAI
34
What is the MC cause of PAI ?
Autoimmune adrenalitis
35
How does Cushing Syndrome affect muscles ?
Muscle atrophy ( due to catabolic effect of cortisol on Muscles) Painless presents as: Proximal muscle weakness
36
What is Cushing syndrome ?
Hypercorticolism
37
Clinical evaluation of cushing
1. 24-hour urine free cortisol / late night salivary cortisol or low-dose dexamethasone test: indicating hypercorticolism then we have to asses if it is ACTH dependent or not so we check ACTH levels. High ACTH --> either pituitary or ectopic (determine by high DMT-suppression test: that would supress ACTH in case of pituitary origin). Low ACTH (adrenal disease or exogenous use)
38
What is cushing disease ?
Hyoercorticolism due to high ACTH production.
39
Primary Hyperaldosteronism or conns syndrome
HTN, Hypokalemia Low renin (due to negative feedback) Metabolic alkalosis (increased excretion of H) Normal Na due to aldosterone escape (HTN, leads to release ATP and Na excretion).
40
Causes of Hyperaldosteronism ?
BIlateral adrenal hyperplasia or Adrenal Adenoma
41
Management of Hyperaldosteronism ?
Surgery, removal of Adenoma or Aldosterone antagonist ( spiro or epleronone) | Epleronone is more mineralocorticoid selective. Less se
42
What are the SE of Spironolactone ?
1. Gynecomastia 2. decreased libido.
43
Clinical Evaluation of Hyperaldosteronism
HTN, Hypokalemia Check PAC/ PRA > 20. ( high aldosterone, low renin). Salt supression: to confirm. Give high amount of salt, lack of supression of aldosterone, confirms diagnosis.
44
Diff. between Central and Peripheral AI ?
central: Low ACTH, low cortisol, normal Aldosterone Peripheral: N ACTH, low Cortisol, low Alodsterone ( Hponatremia, hyperkalemia, and muscle weakness + low Glucose), hyperpigmentation.
45
MC of Central AI ?
Exogenous Cortisol intake and supression of HPA.
46
Diff. between Classical and Non-classical CAH ?
Both have 21-hydroxylase deficiency. Precocious puberty Accumuation of 17-hydroxyprogesterone Classical: salt wasting and hypoglycemia Non-classical: maitain enough cortisol and Aldosterone production.
47
Clinical Evaluation of CAH ?
1. signs of precocious puberty ? 2. ? bone age a. Advanced: check LH i. High LH: Central ii. Low LH --> GnRH stimulation test: LH: increases: central/ LH: no increase: peripheral b. Normal Bone age: Isolated thelarche or adrenarche.
48
What is Pheochromocytoma ?
Catecholamine producing Tumor.
49
CF of pheochromocytoma
HTN, headaches. Paroxysms of severe HTN. Parts of MEN type 1.
50
Management of Pheochromocytoma ?
Alpha blocker first with phenoxybenzamine.
51
Diff. between pheochromocytoma and Thyroid storm ?
Thyroid strom: always with fever.
52
CF of Hyperosmolar Hyperglycemic state
PH normal AG: normal Glucose > 1000 with MS change no ketones | Due to partial deficiency of Insulin
53
Management of HHS ?
Agrresive rehydration with NS (regardless of Na levels) then after than may switch to 0.45% on NS if Na is high.
54
CF of DKA ?
Met. Acidosis with High AG High keta (gamma butyric acid) high glucose of >300 Fruity smell
55
Management of DKA
IV fluids (0.9% NS) Insulin IV ( switch to SC, when Glucose <200, patient able to eat, AG < 12, HCO3 >15) IV potassium Bicarbonate and phosphate
56
Diagnosing DM
Fasting blood glucose > 126 HBA1C > 6.5 Random Blood glucose > 200 OOGT > 200
57
Diagnosing Prediabetes
Fasting blood glucose 100-125 HBA1C 5.7-6.4 Random blood glucose 145-199 OOGT 145-199
58
DD of Hypoglycemia ?
1. beta cell tumors (insulinoma) 2. Exogenous Insulin Intake ( actual insulin or sulfonyl urea: that increases insulin release from Beta cells).
59
Anti-diabetic Agents ?
Metfmron Sulfonyurea (Gliclazide) DDP-4 inhibitors: sitagliptin, vildagliptin GLP-1 agonist: Liraglutide, exenatide
60
SE of Metformin
Lactic Acidosis
61
SE Sulfonylurea
weight gain hypoglycemia
62
Importance of Gliptins or DDP-4 inhibitors
Neutral weight/ no weight gain. Low risk od hypo
63
Patient with Normall fasting glucose but high post-parandial glucose levels?
Need control with short acting insulin post-parandially.
64
Pathophysiology in Refeeding syndrome ?
Starvation/ catabolic state: low insulin, high glucagon, high cortisol leading to catabolism of proteins and fat and their depletion. Refeeding: High insulin High glycogen synthesis, high protein synthesis, cells are hungry so they take all K, phosphorus and magnesium leading to Hypokalemia, hypomagnesemia and hypophosphetemia and low thiamine. Complications: arrythmias, wernicke encephalopathy, and seizures.
65
Effect of mother Hyperglycemia on Fetus
1st trimester: fetus unable to produce insulin --> congenital malformation. 2nd trimester: fetus starts to produce insulin --> hyperinsulinemia --> organomegaly, macrosomia, polycythemia due to increased oxygen consumption. AT birth --> inability to deliver vaginally, shoulder disotcia and Clavicular fracture. After birth --> No more maternal glucose is getting to the fetus, fetus withh suffer from hypoglycemia because of hyperinsulinemia.
66
Insulinoma findings ?
Low glucose High Insulin High Protein c and pro-insulin levels.
67
What is VIPoma
Tumors mainly present in pacreas. secrete Vasoactive intestinal peptide
68
VIP effect ?
Binds to epithelial intestinal wall, increase secrtion of water and K (secretory diarrhea) --> leading to dehydration and muscle weakness (low K). - facial flushing | Part of MEN type 1
69
VIPOMA vs Carcinoid
VIPOMa: in pancrease, Carcinoid: in stomach. Causes diarrhea, flushing and bronchospasm (release of seretonin and Histamine).
70
Cracinoid syndrome leads to deficiency in ?
Niacin ( 3 D: diarrhea, dementia and dermatitis)
71
Pathophysiology behind niacin deficinecy in carcinoid syndrome
Use most tryptophan to produce seretoning. Leading to Tryptophan and niacin deficiancy.
72
Glucagonoma
Mild Diabetes Glucose >500 Diarrhea Erythematous rash with central clearing
73
Diff. b/w Central and Peripheral DI ?
Central: impaired thirst mechanism, sig. hypernatremia Peripheral: Intact thirst mechanism, Normal Na levels
74
CF of DI
Polyuria Polydypsia hypernatremia high serum osmolality low urine osmolality
75
DD of polyuria and polydypsia
1. primary polydypsia: low urine and serum osmolality 2. Central DI: low adh, high serum, low urine osmolality, hypernatremia 3. Nephrogenic DI: resistacnce to ADH, normal Na, high serum, low urine osmolality.
76
DD of Marfan ?
Homocytinuria Ehlers-Danlos Syndrome
77
CF of Homocystenuria
Marfanoid habitus Downward lense subluxation Homocystiene in urine Joint and skin hypermobility
78
CF of wilson ?
1. deposition in basal ganglia ( wing-tremor, wide based gait) 2. kayser-fleischer rings in the eye 3. dystonia, ridgidity
79

Endocrine-NBME (1 decks)

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