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hammer15 Flashcards

1
Q

What happens to sodium levels as glucose increases? Why?

A

Very high glucose leads to low sodium because glyph coast draws out water from the cells and this drowins out the sodium.

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2
Q

How does severe hyponatremia present? Management? Hoe is chronic SIADH treated?

A

Lethargy, seizures, coma. Hypertonic saline, conivaptan, tolvaptan which are ADH antagonists. Demeclocycline which blocks the action of ADH.

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3
Q

Which drugs cause increased potassium release from tissues?

A

Betablockers by blocking uptake, digoxin by blocking Na/K pump and Heparin by blocking aldosterone.

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4
Q

What is the presentation, diagnosis and tratmetn for hyperkalemia?

A

Weqkness, paralysis, ileus, cardiac rhythm disorders. EKG shows peaked T waves, wide QRS, PR prolongation. Abnormal EKG or life threatening hyperkalemia - caclium chloride or calcium gluconate, insulin and glucose, bicarbonate if acidosis caused it (acid goes out, potassium goes into cell). Sodium polystyrene sulfonate (kayexalate) binds and removes K.

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5
Q

What is the presentation and EKG findings of hypokalemia?

A

Weakness, paralysis, loss of reflexes, low magnesium because there are dependent channels. U waves, flattened aT waves and ST depression 2/2 ventricular ectopy.

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6
Q

What are two important causes of metabolic acidosis with a normal anion gap? How can you tell them apart?

A

Renal Tubular acidosis and diarrhea. RTA has a positive urine anion gap while diarrhea has a negative urine anion gap (Na minus Cl)

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7
Q

What is type 1 RTA? What drugs can cause it? What is the pathophysiology, diagnosis and treatment? What is the potassium status?

A

Distal RTA. It is responsible for generating new bicarbonate which is required to secrete acid into tubule. Amphoterocin and other autoimmune diseases damage the distal tubule, hence urine is alkaline (above 5.5 pH). This also leads to increase kidney stones from calcium oxalate. Replace bicarbonate so proximal tubule can absorb a dn correct acidosis. Hypokalemic.

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8
Q

What is type 2 RTA? What drugs can cause it? What is the pathophysiology, diagnosis and treatment? What is the potassium status?

A

Proximal RTA where damage to the proximal tubule decreases the ability of the kidney to reabsorb bicarbonate and it is lost in urine leading to low pH in urine below 5.5. Causes calcium to leech out of bones and osteomalacia follows. Variable urine pH, which stays basic even if bicarbonate is given. Thiazides diuretics to cause volume depletion that enhances bicarbonate reabsorption. Hypokalemic

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9
Q

What is type 4 RTA? What drugs can cause it? What is the pathophysiology, diagnosis and treatment? What is the potassium status?

A

Hyporeninemia, hypoaldosteronism. Most often in Diabetes with decreased effects of aldosterone at kidney tubule. High urine Na despite sodium depleted diet. Has Hyperkalemia. Fludrocortisone.

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10
Q

What acid is formed from methanol overdose?

A

For mic acid

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11
Q

What is the fist step when it is clearer person has nephrolithiasis? What IBD causes nephrolithiasis ? What is the management of stones 5-7 mm? Stones less than 2cm? How is hydronephrosis relieved?

A

analgesic such as ketoralac. Crohn disease due to increase oxalate absorption. Uric acid stones. Nifedipine and tamsulosin to help them pass. Lithotripsy. Stent placement.

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12
Q

How does metabolic acidosis cause stone formation?

A

Removes calcium from bones. Also decreases citrate levels which bind calcium.

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13
Q

What are JNC guidelines for BP in diabetes? Above age 60? What are best initial drugs? When do you use two medications from the start?

A

140/90 . 150/90. Thiazides, CCBs, ACEi or ARBS. If BP is 160/100

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14
Q

Which are pregnancy safe hypertension drugs?

A

BB, CCBs, hydralazine, alpha methyl dopa.

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15
Q

What is the best HTN drugs for coronary artery disease?

A

BB, ACE, ARB

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16
Q

What is the best HTN drugs for diabetes mellitus?

A

ACE, ARB with goal of 140/90

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17
Q

What is the best HTN drugs for BpH? Hyperthyroidism? Osteoporosis?

A

Alpha blocker. Beta blocker. Thiazides

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18
Q

What drugs should you avoid in depression and asthma?

A

Avoid BBs.

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19
Q

What is the rate of BP reduction in hypertensive crisis? What happens if you exceed this rate?

A

10-20% in 1st hour, 5-15% over next 23hours. Can have a stroke.

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20
Q

Which is the best drug for hypertensive crisis which is HTN with end organ damage?

A

Labetalol or nitroprusside (needs monitoring with an Arterial line). Other drugs are Enalapril, CcBs, esmolol, hydralazine.

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21
Q

What are some examples of microcytic anemia? What is the reticulocyte count?

A

Iron deficiency, thalassemia, sideroblastic anemia and ACD. Low reticulocyte count except for alpha thalassemia which gives a high retic count.

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22
Q

When do you transfuse with packed red blood cells?

A

If the patient is symptomatic, if hematocrit is less than 25 in an elderly patient or one with heart disease

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23
Q

When do you give a patient packed red blood cells? How efficient is it?

A

70 to 80% hematocrit due to being concentrated. Each unit of PRBC should raise hematocrit by 3 points per unit or 1g/dL of Hg.

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24
Q

When do you use FFP?

A

Replaces clotting factors in those with an elevated PT, aPTT, iNR or bleeding.

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25
Q

When do you use cryoprecipitate?

A

Replace fibrinogen and has some utility in DIC. Provides high amounts of clotting factors in a smaller plasma volume. Factor 8 and vWF.

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26
Q

What are hepcidin values in ACD? TIBC?

A

Low. High TIBC.

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27
Q

What are leading causes of sideroblastic anemia? Treatment?

A 
Alcohol suppressing bone marrow. Less common causes are lead poisoning, isoniazid, vitamin B6 deficiency.  Vitamin B6 or pyridoxine replacement. Serum Iron: High
Increased ferritin levels
Normal total iron-binding capacity
High transferrin saturation
Hematocrit of about 20-30%
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28
Q

What is unique about Thalassemia?

A

Target cells and normal iron studies.

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29
Q

What is the presentation of alpha thalassemia with 3 genes deleted?

A

Moderate anemia with hemoglobin H which are beta4 tetrads and increased reticulocytes.

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30
Q

What is the presentation of alpha thalassemia with 4 genes deleted?

A

Gamma 4 tetrads or hemoglobin Bart. CHF causes death in utero.

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31
Q

What is the findings in beta thalassemia 1 and beta thalassemia 3?

A

Increased hemoglobin F and A2. Beta thalassemia intermedia with normal hemoglobin F.

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32
Q

What are some causes of B12 deficiency?

A

Pernicious anemia, pancreatic insufficiency, dietary vegan, Crohn disease, celiac, blind loop syndrome, diphyllobothrium latum

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33
Q

What are some causes of Folate deficiency?

A

Dietary deficiency such as Goat milk, psoriasis and skin loss or turnover, phenytoin, sulfa

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34
Q

What are common laboratory anomalies between b12 and folic acid?

A

Megaloblastic anemia. Increased LDH and increased indirect bilirubin, decried reticulocyte count, hypercellular bone marrow, macroovalocytes, increased homocysteine levels.

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35
Q

What value does b12 deficiency have that folate doesn’t have? What is the complication when replacing both of them?

A

Increased Methylmalonic acid. Botha have elevated homocysteine levels. Hypokalemia.

36
Q

How is pernicious anemia confirmed?

A

Anti-intrinsic factor anti-parietal cell bodies.

37
Q

What does B12 need to be absorbed?

A

Pancreatic enzymes to remove B12 from R protein so it can bind with intrinsic factor.

38
Q

When do you use exchange transfusion in severe vasoocclusive crisis?

A

Acute chest syndrome, priapism, stroke, visual disturbance from retinal infarction.

39
Q

What is the first step you should take in a sickle cell patient with acute pain crisis who has a drop in hematocrit?

A

Measure retic count as parvovirus could be a cause.

40
Q

Do steroids and splenectomy work in cold agglutin disease?

A

No.

41
Q

What are findings of G6PD deficiency on peripheral smear?

A

G6PD levels are normal after a hemolytic event. Heinz bodies (seen with methylene blue) and bite cells.

42
Q

What is the pathophysiology of paroxysmal nocturnal hemoglobinuria? What gene is defective?

A

It is a clonal stem cell defect with increased sensitivity of red cells to complement in acidosis. This is from deficiency of complement regulatory proteins CD55 and 59 also known as decay accelerating factor. Defective Phosphatidylinositol gene is defective.

43
Q

What is the presentation of Paroxysmal nocturnal hemoglobinuria? Most common cause of death and treatment?

A

Episodic dark urine, Pancytopenia, clots in unusual places. Thrombosis of mesensteric and hepatic veins. Prednisone for hemolysis, BM transplant for cure, eculizumab to inhibit complement over activation, folic acid.

44
Q

What is the treatment for patients with aplastic anemia who are too old for bone marrow transplant?

A

Antithymocyte globulin and cyclosporine.

45
Q

What is the erythropoietin level in polycythemia Vera? Oxygen level, basophils? MCV? Which drug inhibits JAK2?

A

Low erythropoietin, normal oxygen, low MCV, increased basophils. Ruxolitinib.

46
Q

Which drug suppresses myelofibrosis and which drugs increase bone marrow production?

A

Ruxolitinib inhibits JAK2 and suppresses myelofibrosis. Thalidomide and lenalidomide increase BM production.

47
Q

What is M3 acute leukemia associated with? What is the best initial test? What is characteristic of AML? What medication do you add to M3? To ALL? What is the best indicator of prognosis in acute leukemia?

A

Trans locations between chromosomes 15 and 17. DIC. Best initial test is blood smears showing blasts. Myeloperoxidase and auer rods are characteristics of acute myelocytic leukemia.aTRA to M3 and intrathecal methotrexate to ALL. Good cytogenetics leads to more chemo and less chance of relapse. Bad cytogenetics needs immediate BMT and has more chance of relapse.

48
Q

What is the lab findings in CML? Physical findings? Treatment? What can CML transform to if untreated?

A

High WBC count with all neutrophils. Pruritis from hot shower, splenomegaly. Tyrosine kinase inhibitors such as imatinib, complete cure from BMT. Can convert to acute leukemia. BCR:ABL 9:22.

49
Q

What is the first step in acute leukostasis reaction with highly elevated WBC count?

A

Leukopheresis to remove the excess cells.

50
Q

What is the presentation and diagnostic findings in MDS?

A

Pancytopenia despite a hypercellular bone marrow. Increased MCV, uncleared red cells, ringed sideroblasts, severity based on percentage of blasts.

51
Q

What is the the treatment for myelodysplastic syndrome?

A

Transfusion, erythropoietin, lenalidomide for those with a 5q deletion, bone marrow transplant under age 50. Azacitidine decreases transfusion dependence or decitabine

52
Q

What is the management of patients with elevated serum alkaline phosphatase and direct hyberbilirubenmia?

A

Abdominal US since it could be 2/2 cholestasis

53
Q

What is the next step for patients who have decreased fetal movmement?

A

NST followed by BPP or contraction test is NST is nonreactive

54
Q

What is the presentation of nonalcoholic fatty liver disease? Treatment?

A

Hepatomegaly with mild elevations in liver transaminases and alkaline phosphatase in the absence of other causes of secondary hepatic fat accumulation. Diet and exercise/bariatric surgery if BMI >35.

55
Q

What are the milestones reached by 12 months?

A

Walking independently ,2 finger pincer grasp, saying other words than mama and dada, imitating actions of others

56
Q

What is the pathophysiology of Niemann-Pick disease? Inheritance, onset and clinical features?

A

Sphingomyelinase deficiency. AR. Age 2-6 months. Loss of motor milestones, hypotonia, feeding difficulties, cherry red macula, Hepatosplenomegaly, arreflexia

57
Q

What is the pathophysiology of Tay Sachs disease? Inheritance, onset and clinical features?

A

Hexosaminidase A deficiency. AR. Age 2-6 months. Loss of motor milestones, hypotonia, feeding difficulties, cherry red macula, Hyperreflexia

58
Q

What is the presentation of cholesteatoma?

A

New onset hearing loss or chronic ear drainage despite antibiotic therapy, granulation tissue and skin debris may be seen with retraction pockets of the tympanic membrane on otoscopy

59
Q

What type of abdominal issues do HSP patients have?

A

Ileo-ileal intussusception, abdominal pain, occasional scrotal swelling

60
Q

What is the differential diagnosis for an anterior mediatinal mass? Which germ cell tumors have both AFP and bHCG?

A

4Ts - thymoma, teratoma, thyroid neoplasm, terrible lymphoma. Nonseminomatous germ cell tumors.

61
Q

What is the treatment for acute dystonia 2/2 first gen antipsychotics?

A

Benztropine or diphenhydramine

62
Q

What is the treatment for akathisia, which is a subjective restlessness or inability to sit still?

A

Betablocker or benzodiazepine

63
Q

What is the treatmetn for tardive dyskinesia?

A

No definite treatment, can try Clozapine

64
Q

What can hypertriglyceridemia cause? How is it diagnosed?

A

Acute pancreatitis. Can also have eruptive xanthomas. Fasting serum lipid profile.

65
Q

What is the presentation and etiology of acute hemolytic transfusion reaction?

A

Mismatched blood (ABO incompatability). Fever, flank pain, hemolysis, oliguric renal failure and DIC within 1 hour after transfusion. Positive Coombs

66
Q

What BP meds are used in preeclampsia to lower BP acutely to decrease stroke risk?

A

Hydralazine IV, labetalol IV or nifedipein PO

67
Q

What is the management of chorioretinits?

A

Prompt broad spectrum antibiotics followed by oxytocin to have delivery

68
Q

What is the characteristic of CNS lesions above facial nucleus? Bell’s palsy?

A

Contralateral hemianesthesia or hemiparesis and dysarthria, spares forehead. Bell’s palsy sudden onset of unilateral facial paralysis.

69
Q

What is the characteristic of viral arthritis?

A

Resolves within two months

70
Q

What is the presentation of central precocious puberty? What is treatment?

A

Premature adrenarche, premature thelarche ,advanced bone age. LH is elevated and bone age is advanced. MRI for all cases of elevated LH. Treat with gonadtopin releasing hormone agonist to maximize height velocity by inhibiting FSH and LH release

71
Q

Which oral anticoagulant can you use in acute DVT or PE?

A

Rivaroxaban (direct factor Xa inhibitor), but it has no antidote and works within 2-4 hours.

72
Q

What is the management of patients with acute exacerbation of COPD?

A

Inhaled bronchodilators (beta agoinsts and anticholinergics) and systemic glucocorticoids. Supplemental O2, antibiotics, ventilatory support when indicated

73
Q

What is the management for RLS?

A

Iron supplementation, dopamine agonists (pramipexole) or alpha 2 delta calcium channel ligands (gabapentin)

74
Q

What is the presentation of Wernicke’s encephalopathy? Korsakoff ?Which deficiency?

A

Encephalopathy, oculomotor dysfunction and gait ataxia. Thiamine deficiency. Korsakoff is irreversible amnesia, confabulation and apathy.

75
Q

What renal problems can BPH cause? What do you do to evaluate?

A

Urinary obstruction and renal failure. Renal US to check for hydronephrosis and worsening kidney function.

76
Q

When does free wall rupture occur? Which coronary artery is involved? How does it present and what is seen on echo?

A

Within first 5 days to 2 weeks. LAD. Shock and chest pain, pulseless electrical activity, JVD, distant heart sounds. Pericardial efffusion with tamponade.

77
Q

What methods are used to control confounding?

A

Matching, restriction, randomization

78
Q

What causes appendiceal rupture? Symptoms and treatment?

A

Appendicits > 5 days leading to a contained abscess. Fever, nausea, vomiting, anorexia. hydration, antibiotics, bowel rest and interval appendectomy

79
Q

What is the treatment for vaginismus?

A

Relaxation, Kegel exercise, insertion of objects to encourage desensitization

80
Q

Which electrolyte abnormalities are absorbed in Cushing syndrome?

A

Hypokalemia and hypernatremia

81
Q

What are risk factors for vertebral compression fracture? How does it present?

A

Trauma, osteoporosis or osteomalacia, infection, malignancy. Acute back pain with point tenderness. Pain increases with standing, walking, or lying on the back.

82
Q

What is the prolactin level in prolactinoma and TSH? How is it treated? When do you do surgery?

A

> 200 and normal TSH. If > 1cm or symptomatic, use dopaminergic agonsits (cabergoline, bromocriptine. If treatment fails or tumors are > 3cm, do transphenoidal resection.

83
Q

What is the INR goal for patients with DVT?

A

2 - 3

84
Q

What are the clinical presentation, laboratory findings of immune thrombocytopenia? How are children treated?

A

Prior viral infection, asymptomatic petechiae and echymosis, mucocutaneous bleeding. Isloated low platelets

85
Q

What vitamin deficiency does carcinoid syndrome cause why?

A

Niacin deficiency 2/2 increased seretonin production from tryptophan, but tryptophan is required for niacin synthesis.

86
Q

What rash is typical of mycoplasma? What symptoms does Mycoplamsa PNA present with?

A

Erythema multiforme, atypical PNA with non productive cough and higher extrapulmonary symptoms.

87
Q

What is the presentation of TTP? What is the next step in management?

A

Hemolytic anemia, thrombocytopenia, AMS, renal fialure and/or fever. Schistocytes on peripheral blood smear which is next step.

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