ismailalmokyad's version from 2018-01-22 16:43


Question Answer
1-How to manage suspected ectopic pregnancy?1-if not hemo stable do immediate surgery,
2-if hemo stable do transvaginal US, if ectorpic treat according, if in-uterus leave it, if unclear do BHCG if <1500 repeat Bhcg and us in 2 days if >1500 repeat Bhcg in 2 days.
3-how much does Bhcg increase during first trimester of pregnancy?35% every 2 days during first trimester
4-What is the triad of disseminated gonococcal infection ?1-Dermatitis (2-10 painless pustules on the distal extremities),
2- tenosynovitis ( swelling and pain with passive extension of multiple tendons),
3- polyarthalgia (asymmetric small and large joint arthralgias).

**Fever and maise are also common**
5-How you work-up questionable disseminated gonococcal infection?1-Blood cultures
2-synovial fluid sampling.

Most patient are diagnosed presumptively when nucleic acid amplification testing of urolgenital tract is positive. also one should test for other STD.
6-how to treat neisseria gonorrhea pt and sexual partner of ?test them even if no symptoms. treat with IM ceftriaxone single does and azithromycin single does is added regardless of of chlamydial status.
7-how to treat chlamydia if the patient is allergic to azithromycin ?7 days of doxy
8-how to treat phycosis pt who is not taking his medication?by using long-acting injectable antipsychotics. As first generation (haloperidol and fluphenazine) and many of the second generation.
9-multifocal atrial tachycardia causes, c/p and ttt?1-causes
-electrolyte disturbance
-catecholamine surge(sepsis).

2-C/P asymptomatic, irregular pulse, EKG >3 P wavs & atrial rate >100.

3-ttt is correct underlying causes and AV nodal blockade(verpamil or BB) if persistent.
10-When and how pyloric stenosis present1-age 3-6 weeks
2-first born
4-bottle-fed infancts.
5-nonbloody, nonbilious, projectile vomiting occurs immediately after feeding.
6-dry skin and weight loss.
11-What is the PE finding in pyloric stenosis baby?perstaltic waves traveling from left to right in the upper abdomen after feeding.
12-wt finding suggestive of renovascular disease ?HTN-related symptoms
-Resistant HTN (uncontrolled despite 3-drug regimen)
-Malignant HTN (with end-organ damage)
-Onset of severe HTN (>180/120 mm Hg) after age 55
-Severe HTN with diffuse atherosclerosis
-Recurrent flash pulmonary edema with severe HTN.

Supportive evidence
1-Asymmetric renal size (>1.5 cm)
2-Abdominal bruit
3-Unexplained rise in serum creatinine (>30%) after starting ACE inhibitors or ARBs
4-Unexplained atrophic kidney
13-what are the 2ry cause of HTN wt evidence support there presence1-Renal parenchymal disease
-Elevated serum creatinine
-Abnormal urinalysis (proteinuria, red blood cell casts)

2-Renovascular disease
-Severe hypertension (≥180 mm Hg systolic &/or 120 mm Hg diastolic) after age 55
-Possible recurrent flash pulmonary edema or resistant heart failure
-Unexplained rise in serum creatinine
-Abdominal bruit

3-Primary aldosteronism
-Easily provoked hypokalemia
-Slight hypernatremia
-Hypertension with adrenal incidentaloma

-Paroxysmal elevated blood pressure with tachycardia
-Pounding headaches, palpitations, diaphoresis
-Hypertension with an adrenal incidentaloma

5-Cushing syndrome
-Central obesity, facial plethora
-Proximal muscle weakness, abdominal striae
-Ecchymosis, amenorrhea/erectile dysfunction
-Hypertension with adrenal incidentaloma

-Fatigue, dry skin, cold intolerance
-Constipation, weight gain, bradycardia

7-Primary hyperparathyroidism
-Hypercalcemia (polyuria, polydipsia)
-Kidney stones
-Neuropsychiatric presentations (confusion, depression, psychosis)

8-Coarctation of the aorta
-Differential hypertension with brachial-femoral pulse delay
14-what is the best imaging to diagnose renal artery stenosis-Doppler ultrasound bc risk of due to risk of contrast-induced nephropathy (with CT angiography) and nephrogenic systemic fibrosis (with gadolinium-enhanced MRA).
-Noncontrast MRA may be performed when available.
15-seborrheic dermatitis c/p,risk factor, and treatment1-Clinical features
-Erythematous, pruritic plaques with greasy scales
-Scalp, central face, ears, chest(heavy concentrations of sebaceous glands)

2-Risk factors
-Central nervous system disease (eg, Parkinson disease)

-Topical antifungals (eg, selenium sulfide shampoo, ketoconazole)
-Topical glucocorticoids
-Topical calcineurin inhibitors (eg, pimecrolimus
- keratolytic agents (eg, salicylic acid)

NB-some time relapsing and need retreatment with topical ketoconazole or ciclopirox every 1-2 weeks.
if sever or refractory use oral antifungals (eg, itraconazole, ketoconazole)
16-ttt of scabiesPermethrin
17-Postcholecystectomy diarrhea cause/ cp and treatment1- form of bile salt-induced diarrhea that occurs in 5%-10% of patients following cholecystectomy. primary bile secreted in colon and converted by bacteria to secondary bile that if present in high amount can stimulate colon, after removing gallbladder more 2ry bile can reach colon.

2-intermittent, postprandial, colicky right-upper quadrant abdominal pain. Each bout of pain lasts about 15 minutes.

3-treat with Cholestyramine is a bile salt-binding resin that sequesters excess bile salts and is often effective against this form of diarrhea.
18-wt cause bacterial overgrowth and how to treat it-happen due to anatomic (eg, surgically created blind loops) or motility (eg, diabetes, systemic sclerosis)

-present as abdominal bloating, flatulence, and diarrhea, may be malabsorption syndrome

-treat with antibiotic rifaximin
19-how to manage asymptomatic gall stone that found during pregnancypregnancy increase gall bladder stone formation due to decrease bladder motility and hormone changes related increase concentration of cholesterol in the bile.

if asymptomatic no treatment required as most say asymptomatic and resolve after delivery within 2 months, if symptomatic try treat with fluid and pain meds, if no improvement then cholecystectomy during the 2nd trimester.
20-adrenal insufficiency (Addison's disease) sx, PE, labs, and confirmatory diagnostic labs1-c/p
-weight loss,
-abdominal pain,
-asthenia, amenorrhea,
-poor appetite.

2--Physical examination shows muscle tenderness, decreased axillary and pubic hair (due to decreased adrenal androgen production), and increased pigmentation (due to co-secretion ACTH and melanocyte-stimulating hormone if primary adrenal insufficiency)

2-hyperCL metabolic acidosis
4-hypoglycemia (or borderline)

1-measurement of a morning plasma cortisol and ACTH; low cortisol with elevated ACTH is diagnostic for primary adrenal insufficiency.
2-If results are equivocal do ACTH stimulation test ( 250 mic of cosyntropin) and repeat cortisone and ACTH.
3-if both basal cortisol and ACTH are low and suboptimal cortisol response to cosyntropin then this is secondary or tertiary adrenal insufficiency.
4- normal cortisol level (>20 mic) 30-60 min after cosyntropin indicate that adrenal insufficiency and one should look for different explanation.
5- if still indeterminate do imaging to the pituitary.
21-wt is tinea versicolor, cp, dx, ttt-fungal infection of the skin caused by Malassezia species
multiple, often coalescing, small circular maculae that may vary in color (white, pink, or brown) may be very mild itching.

dx-potassium hydroxide (KOH) preparation showing hyphae and yeast.

ttt:topical anti-fungal therapy (eg, selenium sulfide, terbinafine, clotrimazole, ketoconazole).
-With extensive disease or recalcitrant infection, oral antifungals (ketoconazole, itraconazole, or fluconazole) are preferred.

NB:Topical terbinafine is effective, but oral terbinafine and oral griseofulvin are ineffective
22-polymyalgia rheumatica, symptoms, physical, labs and ttt-Age >50
-B/L pain & morning stiffnes>1 month, plus 2 of the following
1-neck or torso
2-shoulders of proximal arms
3-hip or proximal thighs
4-constitutional (fever, malaise, weight loss).
5-cant find comfortable position at night.

-physical showes decrease ROM in affected joints

2-elevated CRP
3-normocytic anemia
4-20% normal
5-normal CK and aldolase

ttt- glucocorticoids (all pt response to it, if not look for different dx)
-low does (prednisone 10-20 mg daily)
-if associated with giant cell arteritis then high does (prednisone 40-60 mg daily)
23- what disease is associated with polymyalgia rheumaticafrequently associated with giant cell arteritis (GCA)
24- constitutional delay of growth and puberty VS familial short stature-constitutional delay of growth and puberty has a delay in puberty, normal growth velocity (4-6 cm/yr). constitutional delay is associated with a delayed bone age on x-ray of the wrist

NB:Puberty is considered delayed if no secondary sexual characteristics (typically testicular enlargement [>4 mL] or breast development) are present by age 14 in boys or age 12 in girls.

-In contrast to familial short stature, in which short stature and normal growth velocity are accompanied by a normal bone age,

-Reassurance; watchful waiting
-± Hormone therapy

-Puberty onset correlates with family members
-Normal expected adult height
-If psychosocial concerns are severe, or if puberty is significantly delayed, short-term testosterone therapy in boys, or estrogen therapy in girls, may be considered. Pharmacotherapy, however, should be used only in boys age >14 or girls age >12.
25-labs, dx, and ttt of paget's diseaselabs
-elevated serum bone-specific ALP
-normal Ca and pho

-with labs and imaging
-bone scan is more senstive than xray and can locate all the involved bones.
-CT can show thickened areas with cotton wool appearance

ttt with bisphosphonates espicially if bone pain or high risk bone as skull.
26-wt patterns of calcificaton within pulm nodule suggest benign and wt suggest malignantbenign :popcorn, concentric or laminated, central, and diffuse homogeneous calcifications.

Eccentric calcification (area of asymmetric calcification), as well as reticular or punctate calcification, should raise suspicion for malignancy
27-wt is the difference between T1DM and chronic pancreatitis induced DMPD are prone to developing hypoglycemia due to loss of glucagon-producing alpha cells in addition to the loss of beta cells. (In type 1 diabetes, there is loss of beta cells, only). but loss of glucagon secretion, make diabetic ketoacidosis rare in PD
28-how to treat different type of conjunctivitis (bacterial, viral, allergic)1-Bacterial conjunctivitis (Staphy aureus, Strep pneumoniae, Moraxella catarrhalis, and Haemophilus influenzae)
-Erythromycin ointment
-Polymyxin-trimethoprim drops
-Azithromycin drops
-Preferred agent in contact lens wearers: fluoroquinolone drops as ciprofloxacin, ofloxacin ( pseudomonas risk)

-self-limited, but topical antibiotics are prescribed to shorten symptom duration and reduce person-to-person transmission.

2-Viral conjunctivitis
-Warm or cold compresses
-± Antihistamine/decongestant drops

3-Allergic conjunctivitis
-Over-the-counter antihistamine/decongestant drops for intermittent symptoms
-Mast cell stabilizer/antihistamine drops for frequent episodes
29-wt is the complication of bacterial conjunctivitis, cp, risk, dx and ttt of this complicationbacterial keratitis ( inflammation of the cornea) most commonly occurs in patients who wear contact lenses improperly (eg, overnight use) or have decreased immunity (eg, corticosteroid use).

presents with photophobia, blurred or impaired vision, and a foreign body sensation with difficulty opening the affected eye.

should be seen urgently by an ophthalmologist to confirm the diagnosis and begin treatment.

management slit-lamp examination showing corneal ulceration, Cultures of corneal scraping should be obtained to help guide definitive antibiotic therapy. While those cultures are processing, empiric therapy should be changed to topical, combination antibiotic therapy that has broad-spectrum activity against gram-positive and gram-negative organisms, including Pseudomonas. Keratitis can cause scarring or ulceration of the cornea and subsequent blindness if not aggressively treated.
30- wt is Hordeolum (stye)bacterial infection of the sebaceous glands in the eyelid. Patients have tenderness, redness, and swelling at the eyelid margins

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