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MCCEE > Endo > Flashcards

Endo Flashcards

1
Q

Type of inheritance in familial hyper cholesterolemia?

A

Autosomal co-dominance with high penetrance.

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2
Q

What is the defect in familial vs polygenic hyper cholesterolemia?

A

Familial: Defect in LDL receptor on cell membrane.

Polygenic: Defect in cholesterol metabolism.

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3
Q

Labs in familial vs polygenic hypercholestrolemia?

A

Both show high TC + LDL

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4
Q

Clinical presentation in familial vs polygenic hyper cholesterolemia?

A

Familial:
Lipid deposits => tendinous xanthomatosis + xanthelasmata + arcus cornealis

Polygenic:
Asymptomatic

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5
Q

Risk of CAD in familial hypercholestrolemia. (Heteo vs homo)

A

Heterozygotes: 50% risk of MI in men by age 30

Homozygotes: CAD and vascular disease early in childhood

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6
Q

Rx of familial (hetero/homo) vs polygenic hypercholestrolemia.

A

Hetero Familial: HMG-coA reductase inhibitors + niacin / ezetimibe / bile acid sequestrant

Homo familia: portocaval shunt or LDH apheresis + niacin / atorvastatin

Polygenic: HMG-CoA reductase inhibitors, ezetimibe, niacin or bile acid sequestrant

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7
Q

Causes of 2ry hypercholestrolemia?

A 
Endo: hypothyroidism
Renal: nephrotic syndrome
Hepatic: PBC
Immune: monoclonal gammopathy
Diet: anorexia nervosa
Drugs: cyclosporin + carbamazepine + anabolic steroids.
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8
Q

What are the syndromes of 1ry hyper-Triglyceridemia?

A
  1. Familial lipoprotein lipase deficiency

2. Familial hyper-triglyceridemia

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9
Q

Pathophysiology of familial lipoprotein lipase deficiency vs familial hyper-triglyceridemia?

A

Familial lipoprotein lipase: deficiency or lipoprotein lipase or its co-factor.

Familial hyper-TG: increased hepatic VLDL production or decreased VLDL clearance.

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10
Q

Lab findings in familial lipoprotein lipase vs familial hyper-TG?

A

Familial lipoprotein lipase: high TG, VLDL, chylomicrons.

Familial hyper-TG: high TG + VLDL

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11
Q

Sx of familial lipoprotein lipase vs hyper-TG?

A 
1.Familial lipoprotein lipase: 
Hepatosplenomegaly + splenic infarcts => anemia, granulocytopenia, thrombocytopenia. 
Pancreatitis
Lipemia retinalis 
Eruptive xanthomata
  1. Familial hyper-TG:
    Premature CAD
    Syndrome of obesity, high TG, high insulin, high urea.
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12
Q

Treatment of familial lipoprotein lipase vs familial hyper-TG?

A
  1. Familial lipoprotein lipase:

Fat intake

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13
Q

When is hyper-triglyceridemia associated with pancreatitis?

A

When Serum TG > 1000 mg/dL

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14
Q

Drugs cause 2ry hyper-Triglyceridemia?

A 
Alcohol
Steroids 
Estrogen
OCP
Hydrochlorothiazide
Retinoic acid
Anti-retrovials
Atypical antipsychotics
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15
Q

Side effects of atypical antipsychotics?

A

Dyslipidemia
HTN
Hyperglycemia
Metabolic syndrome

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16
Q

Types of combined hyperlipidemia?

A

Both 1ry.

  1. Familial combined hyperlipidemia
  2. Dysbetalipoproteinemia
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17
Q

Path physiology of familial combined hyperlipidemia vs Dysbetalipoproteinemia?

A
  1. Familial combined:
    Excess hepatic synthesis of ApoB
  2. Dysbetalipoproteinemia: abnormal ApoE
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18
Q

Labs in familial combined hyperlipidemia vs Dysbetalipoproteinemia?

A
  1. Familial combined: high TC, TG, VLDL, LDL

2. Dysbetalipoproteinemia: high TC, TG, VLDL, IDL

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19
Q

Sx of familial combined hyperlipidemia vs Dysbetalipoproteinemia?

A
  1. Familial combined:
    CAD
    Xanthelasma
  2. Dysbetalipoproteinemia:
    Tuberous, eruptive, palmar xanthomata
    Impaired glucose tolerance
    CAD + PAD.
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20
Q

Rx of familial combined hyperlipidemia vs Dysbetalipoproteinemia?

A 
Both:
Weight reduction 
Low fat, carbs intake + stop EtOH
HMG-CoA reductase inhibitors
Niacin, fibrates
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21
Q

Types of dyslipidemias?

A

Hyper cholesterolemia

Hyper triglyceridemia

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22
Q

When to screen to dyslipidemias?

A
  1. Healthy men at 40 women after menopause.
  2. Children with FHx
  3. At any age if patient has:
    - DM
    - HTN
    - Smoker
    - Obese
    - Sx of hyperlipidemia (xanthomata, arcus cornealis)
    - FHx of premature CAD
    - Atherosclerosis
    - Rheumatoid arthritis / SLE / psoriasis
    - HIV on HAART
    - CKD (GFR
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23
Q

What’s the effect of high LDL on CAD risk?

A

Each 40mg/dL (1 mmol/L) reduction in LDL = 20% relative risk reduction in CAD.

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24
Q

Labs for statin F/U?

A
  1. Liver profile: before Rx and after initiation.
  2. Lipid profile: after stabilization check annually.
  3. CK at baseline + if patient complains of myalgia.
    NB: D/C statins if CK>10x upper limit.
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25
Q

Define Diabetes Mellitus.

A

Inappropriate hyperglycemia 2ry to insulin deficiency and/or reduction in its biological effectiveness.

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26
Q

Types of primary hypertricholestrolemia?

A

Familia and polygenic

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26
Q

Age of indent in T1DM + T2DM?

A

T1DM less than 30

T2DM more than 40

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27
Q

Psychophysiology of T1DM vs T2DM?

A
  1. T1DM:
    Autoimmune
    Genetic, immune, environmental factors => B-cell destruction via infiltration with lymphocytes.
    80% cells destroyed before Sx
  2. T2DM:
    - multi factorial
    Impaired insulin secretion, peripheral insulin resistance and excess hepatic glucose production.
    NB: resistance 2ry to receptor abnormalities.
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28
Q

Genetics in T1DM vs T2DM

A
  1. T1DM:
    Associated w/ HLA-DR3 + DR4 + DQ
  2. T2DM:
    No HLA association
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29
Q

What acute complications occur in diabetes?

A

Diabetic ketoacidosis DKA

Hyperosmolar hyperglycemic state HHS

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30
Q

Path physiology of DKA vs HHS

A
  1. DKA:
    Lack of insulin => high stress hormones (glucagon, cortisol, catecholamines, GH).

Stress hormones => cont hepatic glucose > hyperglycemia > osmotic diuresis > dehydration + electrolyte imbalance (low Na | high K)

FFA metabolism to make glucose => ketoacids > metabolic acidosis.

Sever hyperglycemia + ketone = glucosuria + ketonuria.

  1. HHS
    After stress => High stress hormones

Stress hormones => high hepatic glucose production > hyperglycemia > osmotic diuresis > dehydration.

Bcz insulin is present => no need for lipolysis => no ketones.

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31
Q

Explain decreased LOC / coma in DKA + HHS

A

Volume contraction => renal insufficiency > hyperglycemia + high osmolality > fluid shift from neurons to ECF > coma.

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32
Q

Sx of DKA vs HHS

A 
1. DKA:
Polyuria, polydipsia, polyphagia + fatigue + N/V
Abdominal pain 
Dehydration
Low LOC / Coma 
Fruity smelling breath
Kussmaul's respiration
2. HHS:
Polyuria, polydipsia, weakness 
Dehydration
Low LOC / coma 
Kussmaul's respiration 
Hx low fluid intake + ingestion of glucose containing food.
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33
Q

Labs of DKA vs HHS?

Serum, ABG, urine

A 
1. DKA:
Serum =>
- hyperglycemia >200
- pseudohyponatremia
- high K
- low HCO3
- high BUN + Cr
- low PO4
- High osmolality

ABG =>
Metabolic acidosis with high AG
+/- respiratory alkalosis or metabolic alkalosis (sever vomiting)

Urine =>
Glucosuria + ketonuria

2. HHS:
Serum =>
- hyperglycemia > 200
- hypo or hyper natermia. 
- high osmolality

ABG =>
Normal unless the stressor causes acidosis eg: lactic acidosis in MI.

Urine =>
Glycosuria

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34
Q

Rx of DKA vs HHS?

A
  1. DKA:
    - ABC + monitor acidosis with ABG
  • Rehydration:
    • 1st 2 hr > NS at 1L/h
    • Then 0.45 NaCl at 300-400 ml/hr
    • If glucose ~250 => start D5W
  • Insulin:
    • maintain on 0.1 U/kg/h regular insulin
    • DO NOT use with low K.
    • Check glucose hourly.
  • K replacement:
    • develops 2ry to insulin
    • in K hold insulin + K 40 meq/L
    • if K 3.5 - 5 => KCL 20-40 meq/L IV

NB: use HCO3 if PH 7.1

2. HHS:
ABC
- Rehydration:
• NS 1L/hr for 1 hour. 
• Then check Na:
high/normal Na > 0.45 NaCl at 4-14 ml/kg/hr
Low Na > cont NS at 4-14 ml/kg/hr
• If glucose ~250 => switch to D5W
  • Insulin
    • Loading dose = 0.1 U/kg bolus
    • Infusion regular insulin at 0.1 U/kg/hr
    • check glucose hourly
  • K replacement
    • K
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35
Q

Causes of ketoniema?

A

DKA
Alcohol ketosis
Starvation

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36
Q

Complications of DM (macro + micro)

A
  1. Macrovasculr:
    • CAD:
    3-5x higher risk of MI

• stroke:
2.5x higher risk.

• PAD:
Intermittent claudication, intestinal angina, foot ulcers.
30x higher risk of foot gangrene + 15x higher risk of amputations

  1. Micro vascular:
    • Retinopathy:
    T1DM => 25% affected at 5yr + 100% at 20 yrs
    T2DM => 25% affected at Dx + 60% at 20 yrs

• Nephropathy:
T1DM => 20-40% after 5-10 yr
T2DM => 4-20%

• Neuropathy
50% of T1DM + T2DM at 10yrs
Sensory + motor + autonomic

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37
Q

What’s C-peptide? How does it distinguish endogenous vs exogenous insulin?

A
  1. It’s peptide released when pro-insulin cleaved into insulin
  2. High C-peptide = endogenous
    Low C-peptide = exogenous
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38
Q

Causes of hypoglycemia?

A
  1. Fasting:
    - hyperinsluinism:
    Exogenous insulin
    Sulfonylurea or meglitinide reaction
    Pentamidine
    Autoimmune hypoglycemia
    Insulinoma
- Non-hyperinsluinism:
Hepatic dysfunction 
Renal failure
High cortisol 
Alcohol 
Non-pancreatic tumor 
2. Post-prandial:
GI tract 
Occult DM
Fructose intolerance 
Galactosemia 
Newborn of DM mom
39
Q

What’s a pituitary adenoma?

A

Benign slow growing tumor of pituitary gland

39
Q

Sx of hypoglycemia? (Whippel’s Triad).

A
  1. Glucose ranges less 45-40 (2.2-2.5)
  2. Neuroglycopenic Sx
  3. Rapid relief after glucose
40
Q

Classification of pituitary adenoma?

A

Microadenoma 1cm
Functional = secretory
Non-functional = not secretory

41
Q

Sx of pituitary adenoma?

A
  1. Mass effects
    Headache
    Bitemporal
42
Q

Investigation of pituitary adenoma?

A

Hormones tests (PRL, TSH, 8AM cortisol, FSH/LH, IGF-1, fasting glucose)

MRI w/o contrast (image of choice)

Visual field test

43
Q

Causes of hypopituitarism? (8 I’s)

A

8 I’s:

  • Invasive:
    Tumor, craniopharyngioma, cysts (Rathke’s | dermoid | arachnoid)
  • Infarction:
    • Sheehan
    • apoplexy
  • Inflammatory:
    Sarcoidosis, histiocytosis, hemochromatosis
  • Infectious:
    TB, syphilis, toxo
  • immune: autoimmune destruction
  • iatrogenic
  • Injury
  • Idiopathic
44
Q

Investigation for hypopituitarism?

A

Triple bolus test

45
Q

Sx of hyperthyroidism?

A

THYROIDISM:

Tremor 
HR up
Yawning (fatigue)
Restlessness
Oligomenorrhea/amenorrhea
Intolerance to heat
Diarrhea 
Irritability 
Sweating 
Muscle waiting / weight loss.
46
Q

DDx of thyrotoxicosis?

A
  1. Hyperthyroidism:
    - Graves Dz
    - Toxic nodular goiter
    - Toxic nodule
  2. Thyroiditis:
    - subacute, Silent, post-partum
  3. Extra-thyroidal hormone:
    - Endogenous: ovarian teratoma, met follicular carcinoma
    - Exogenous: drugs
  4. Excessive Thyroid production:
    - pituitary thyrotophoma
    - pituitary T4 receptor resistance
    - high hCG (pregnancy)
47
Q

Define Graves Disease?

A

Autoimmune disorder with antibodies to TSH receptor leading to hyper thyroidism

48
Q

Genetics of Graves’ disease?

A

Associated with HLA-B8 + DR3

49
Q

What’s the most common cause of thyrotoxicosis?

A

Graves’ disease

50
Q

Pathophysiology of Graves Disease?

A
  • autoimmune defect in T- suppressor cells

B lymphocytes > TSI > stimulate gland.

51
Q

What triggers Graves’ disease?

A

Postpartum state
Viral or bacterial infection
Drug: iodine or lithium
Glucocorticoids withdrawal.

52
Q

Sx of Graves’ disease?

A 
Sx of thyrotoxicosis 
Diffuse goiter + bruit
Ophthalmology 
Dermopathy
Acropachy
53
Q

What ophthalmopathy seen in Graves’ disease by order? (NO SPECS)

A
  • No signs
  • Only: Lid lag + lid retraction
  • Soft tissue: puffiness, conjunctival injection, chemosis
  • Proptosis/exophthalmos
  • Extra ocular (diplopia)
  • Corneal abrasion (cuz can’t close eyes)
  • Sight loss.
54
Q

What causes ophthalmopathy and dermopathy in Graves’ disease?

A

Deposition of glycosaminoglycan

55
Q

Rx of Graves’ disease

A
  1. Anti-thyroid drugs = thionamides.
    PTU or Methimazole
    Cont until remission (at 6 mo)
    NB: MMI better than PTU cuz longer action.
  2. Thyroid ablation if PTU/MMI fail.
  3. Sx treatment via B-blockers
  4. Thyroidectomy for large thyroid.
    Risk of vocal cord palsy.
56
Q

Mechanism of action of PTU + methimazole?

A

Inhibit peroxidase-catalyzed reactions => no iodide organification => no iodotyrosine coupling.

PTU also stops peripheral deiodination of T4 to T3.

57
Q

Side effects of PTU + Methimazole?

A

Hepatitis
Agranulocytosis
Fever / arthralgia
Rash

MMI is teratogenic in 1st trimester

58
Q

Natural Hx of subacute thyroiditis?

A

Initial thyrotoxic state > hypothyroidism > euthyroidism.

59
Q

Pathophysiology of subacute thyroiditis?

A

Acute inflammation by giant cells + lymphocytes => disruption of thyroid follicles => release of stored hormones.

60
Q

Subtypes of subacute thyroiditis?

A
  1. Painful (De quervian’s)

2. Painless (silent)

61
Q

Causes of subtypes of subacute thyroiditis?

A
  1. Painful:
    • viral or URTI
    • granulomatous thyroiditis
  2. Painless
    • post-partum
    • autoimmune
    • lymphocytic.
62
Q

Sx of painful subacute thyroiditis?

A
  • thyroid, ear, jaw, occipital pain.

- fever + malaise in granulomatous

63
Q

When dose post-parting thyroiditis occur?

A

2-3 mo after delivery

64
Q

Rx of subacute thyroiditis?

A
  1. Painful:
    • High dose NSAIDs
    • Prednisone for sever pain, fever, malaise.
  • iodinated contrast agents (ipodate | iopanic acid)
  • BB for Sx hyperthyroid
  • thyroxin if hypothyroid
65
Q

What is the prognosis in subacute thyroiditis thyroiditis?

A

Full recovery, permanent hypothyroid in 10%.

66
Q

Rx of toxic nodular goiter?

A
  1. Surgical removal
  2. PTU or MMI
  3. Radioactive ablation
67
Q

Define thyroid storm

A

Acute exacerbation of all symptoms of thyrotoxicosis in a life-threatening state.

68
Q

Patio physiology of thyroid storm

A

Excessive stimulation of thyroid hormones in hyperthyroid patient due to stress (infection, trauma, surgery)

69
Q

Signs of thyroid storm?

A 
Hyperthyroidism 
Extreme hyperthermia 
Tachycardia + CHF
Vomiting + diarrhea
Vascular collapse + shock 
Delirium + coma
70
Q

Rx of thyroid storm?

A

PTU is drug of choice

  • give iodide 1hr after PTU
  • DXS 2-4 mg IV q6hr for 48hr.
71
Q

What is the most common cause of primary hypothyroidism?

A

North America: Hashimoto’s

World: low iodine

72
Q

What are forms of Hashimoto’s thyroiditis? (2)

A
  1. Goitrous

2. Atrophic

73
Q

Pathophysiology of Hashimoto’s?

A

Defect in T suppressors => cell medicated destruction of thyroid follicles via b lymphocyte antibodies.

Ab against => thyroglobulin, thyroid peroxidase, TSH receptor

74
Q

Association with Hashimoto’s?

A

Down’s syndrome
Turner’s
Cytotoxic T lymphocyte associated protein 4 (CTLA-4)

75
Q

What is sick euthyroid syndrome?

A

Changes in circulating thyroid hormones in patients with serious illness not due to intrinsic thyroid or pituitary disease

76
Q

What is pheochromocytoma?

A

It is a catecholamine secreting tumor derived from chromaffin cells of the sympathetic system in adrenal medulla.

77
Q

What is the classic triad of pheochromocytoma? (PHE)

A

Palpitation, headache, episodic sweating.

78
Q

What are the associations with pheochromocytoma?

A
  1. Multiple endocrine neoplasia II (Men IIA + IIB)
  2. Von Hippel-Lindau
  3. Paraganglioma
  4. Neurofibromatosis-1
79
Q

Sx A pheochromocytoma?

A
  1. HTN or orthodontic hypotension
  2. Classic triad palpitation, sweating, headache.
  3. Others: tremor, anxiety, N/V, blurred vision
80
Q

Labs in pheochromocytoma

A
  1. Urine catecholamines:
    High free catecholamines and Metanephrines.
  2. CT abdomen (if -ve => total body)
81
Q

Rx of pheochromocytoma?

A

Surgical removal is curative.

82
Q

Preoperative preparation of pheochromocytoma?

A
  1. Alpha blockers for BP control
    2 Beta blockers for HR control
  2. Metyrosine + phenoxybenzamine.
  3. Volume restoration.
  4. Re-screen urine 1-3 mo post-op
83
Q

Causes of primary secondary and tertiary Hyperparathyroidism?

A
  1. Primary:
    Parathyroid adenoma
    Lithium
    Carcinoma
  2. Secondary:
    Partial PTH resistance (renal failure + osteomalacia).
  3. Tertiary:
    Irreversible clonal outgrowth of parathyroid gland.
84
Q

Most common cause of hypercalcemia (healthy bs hospitalized)?

A
  • Healthy = Primary Hyperparathyroidism.

- Hospitalized = Cancer.

85
Q

Rx of primary Hyperparathyroidism?

A

Surgery is curative only if symptomatic

86
Q

When is surgery recommended for Asymptomatic 1ry Hyperparathyroidism?

A

if has 1 ore more of the following:

  • Ca is 1.0 mg/dL above upper limit
  • Cr clearance
87
Q

Ca levels in hypercalcemia (corrected + ionized).

A

Corrected > 10.5 mg/dL (2.6 mmol/L)

Ionized > 5.4 mg/dL (1.35 mmol/L)

88
Q

How to correct Ca?

A

Measured Ca + 0.02 (40-albumin)

NB: for every decrease in albumin by 10, increase of Ca by 0.2

89
Q

Symptoms of hypercalcemia?

A

Bones stones groans and psychic overtones

GI: N/V, constipation
Renal: polyuria, stones, failure.
MSK: weakness, bone pains, gout/pseudo gout
Psych: anxiety, depression

Neuro: hypotonia, hyporeflexia, myopathy
CVS: HTN, arrhythmia, short QT

90
Q

Rx of acute hypercalcemia?

A
  1. Increase urinary excretion:
    • volume expansion = NS 500 cc/hr.
    • loop diuretics (only if hypervolemic
    • Calcitonin
  2. Diminish bone resorption:
    • Bisphosphonate (Rx of choice)
  3. Decrease GI absorption:
    • Corticosteroid:
    Most useful in vitD toxicity, granulomatous disease.
  4. Dialysis
    Sever malignancy-associated hypercalcemia
91
Q

Causes of low PO4?

GI, Randal, MSK

A
  1. GI:
    Antacid
    Alcohol
    Malabsorption
2. Renal:
Hyperparathyroidism 
Rickets
Fanconi
Multiple myeloma 
Recovery of metabolic acidosis
  1. MSK:
    Hungary bone syndrome
92
Q

Normal level of PO4?

A

2.4 - 4.1 mg/dL (0.85-1.45 mmol/L)

93
Q

Normal Mg levels?

A

1.7 - 2.1 mg/dL (0.7 -0.85 mmol/L)

94
Q

Sx of low Mg?

A 
Chvostek + Trousseau 
Torsades de pointes
ECG: wide QRS, long PR, T-wave 
Seizure 
Paralysis.

MCCEE (3 decks)

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