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ismailalmokyad's version from 2018-01-22 14:57

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Question Answer
1-wt is cause bicuspid aortic valve?autosomal dominant with incomlete penetrance or can be sporadic
2-wt is the prevelance of bicupid aortic valve1% of population, more in male, 30% of pt with turner syndrom.
3-wt are the complications of bicuspid aortic valve1-infective endocarditis
2-refurgitation/stenosis
3-aortic root or ascending aortic dilation or dissection.
4-what is the management of bicuspid aortic valvefollow up echo every 1-2 year, and screening for first relavtive, balloon valvuoplasty or surgery(valve or ascending aorta replacement)
5-What are the congenital conditions associated with bicuspid aortic valve1-coarctation of aorta
2-ascending aortic aneurysm
3-coronary artery anomaly of origin
4-supra or subvalvular stenosis
5-VSD
6-sinus of valsalva
6-wt is the indication of balloon valvuloplasty in bicuspid aortic valvesymptpmatic or asymptomatic (if want to become pregnant of participate in competitive sports) when the following criteria are met: aortic stenosis, no regurgitation or calcification, and peak gradient of >50 mm hg
7-how to manage hypoglycemia1- confirm it is true hypoglycemia with positive Whipple's triad
-symptoms of hypoglycemia
-low blood glucose
-symptom resolution after glucose administration.

2-measure blood insulin, c-peptide, and proinsulin
-if insulin elevated and c-peptide and proinsulin are low then this is exogenous insulin.
-if all elevated this is endogenous insulin induced by oral hypoglucemic agent or insulinoma. first do hypoglycemic drug assay(see if he is taking oral meds), if negative then do u/s or ct to localize the insulinoma for resection.
8-special consideration when evaluate hypoglycemiaNB:when evaluate hypoglycemia
1-whipple's triad must be positive as some ppl run low any way
2-hypoglycemia must suppress insulin, proinsulin and c-peptid, if normal or elevated this is abnormal
3-fingerstick is not accuret in hypo, so do serum to confirm
4-obtain blood sample before given glucose is given.
5-in pt with normoglycemic state and suspected hypoglycemic disorder do 72 hour fasting test to induce hypoglycemia.
9-what is late-life depression and what condition associatd with it ?-it is depression occur at age >65 year old, reversible cognitive impairment (pseudodementia). usually if depression treated demintia improve significantly
-it is risk factor for major neurocognitive disorder (dementia as Alzheimer) in the years to follow.
10-what is symptoms of hypoCa and wt are the DD and what is lab finding in each one of them****Symptoms:
-symptoms neuromuscular excitability (tetany)
-seizures
-muscle cramping
-paresthesias
-hyperreflexia
-laryngospasm.

****Other findings
-cardiotoxicity (eg, heart failure, QT prolongation)
-psychosis (eg, anxiety, depression).
-Dysmorphic features (eg, short stature, round facies, short 4th/5th metacarpals) are present in a subtype of pseudohypoparathyroidism known as Albright hereditary osteodystrophy (resistance to PTH).

****Causes and labs finding:
1-Vitamin D deficience
-Low pho
-High PTH

2-Hypoparathyroidism
-High pho
-Low PTH

3-Pseudohypoparathyroidism (like albright hereditary osteodystrophy)
-High pho
-High PTH

4-Hyperphosphatemia (like in ESRD)
-High pho
-High PTH
11- wt is primary and secondary cause of headache and what is the headache red flags and what are the common disease associated with it-primary migraine, tension, cluster
-secondary: tumor, infection, vascular..etc, present with red flag symptoms:

-Red flag symptoms and associated conditions are
1-Sudden onset, worst headache of life
-Subarachnoid hemorrhage

2-Age >40
-Mass lesion
-Giant cell arteritis

3-Increased frequency or severity
-Mass lesion
-Subdural hematoma
-Medication overuse

4-Worsened by exercise or sexual intercourse
-Mass lesion
-Subarachnoid hemorrhage

5-Focal neurologic signs, papilledema
-Mass lesion
-Idiopathic intracranial hypertension (pseudotumor cerebri)
-Arteriovenous malformation

6-Personality changes
-Central nervous system infection
-Mass lesion
-Intracerebral hemorrhage

7-Systemic symptoms (eg, fever, rash)
-Encephalitis
-Meningitis
12-papilledema common causes?common causes.
-Mass lesions
-Cerebral edema
-Increased cerebrospinal fluid (CSF) production
-Decreased CSF outflow (venous thrombosis)
-Idiopathic intracranial hypertension (pseudotumor cerebri)
13-how to screen for hcv infection-first do HCV antibody testing positive test mean:
1-Active, ongoing infection (chronic or acute)
2-Past infection that has resolved
3-False-positive result

- if positive further do HCV nucleic acid testing (NAT) to detect HCV RNA in the blood.
- if RNA positive the identify the HCV genotype and the extent of liver fibrosis (eg, liver biopsy)
- treat with antiviral therapy.
14-acute pancreatitis causes, c/p, dx, ttt, complication1-Etiology
-Chronic alcohol use
-Gallstone disease
-Hypertriglyceridemia,
-Hypercalcemia
-Drugs (eg, valproic acid, diuretics)
-Infections (eg, CMV, HIV, ascariasis)
-Trauma, ischemia, post-ERCP

NB: to identifiy the cause exclude gallstones and alcohol (65%), if negative do lipids(1-4%)

2-Clinical presentation
-Acute epigastric pain radiating to the back
-± Fever, nausea, vomiting
-Tachypnea, hypoxemia, hypotension if severe

3-Diagnosis Requires 2 of the following:
-Characteristic epigastric pain
-Serum amylase or lipase >3 times normal
-Imaging findings consistent with pancreatitis (contrast CT, MRI, U/S), us is best but if uncertainty or suspected complications of AP then do CT or MRI.

4-Treatment
-Aggressive intravenous volume resuscitation
-Pain control (eg, hydromorphone)
-Nothing by mouth until pain resolves, nasojejunal feeds if oral intolerance >3-4 days

5-complication:
1- pseudocysts: fluid collection one month post symptoms, mostly incident finding but may cause indigestion and pain. if symptomatic treat with needle aspiration.
2- infected pancreatic necrosis(2-6 weeks): ischemia lead to necrosis that can be infected and almost always fatal. treat with IV abx and remove necrotic tissue.
3-SIRS
4-chronic pancreatitis
do CT >72 hours of presentation.
15-what is the most common disease assocaited with OSAobesity hypoventilation syndrome
16- how to manage pt with CHF and pulm edema if diuretics is not workingif inadequate response then use nitroglycerin to induce venous dilation and decrease preload and reduce intracardia filling pressure.
17-how to dx bacterial vaginosis and how to treat-When 3 of the following criteria are present:
1-Homogeneous vaginal discharge(Thin, off-white discharge with fishy odor,No vaginal inflammation)
2-Vaginal pH >4.5
3-Amine odor after application of potassium hydroxide(whiff test)
4-Clue cells (epithelial cells covered in bacteria) on wet mount microscopic examination

-treated with oral or vaginal metronidazole or clindamycin

-complication
-if pregnant:
1-↑ Risk of preterm birth,
2-preterm ROM,
3-chorioamnionitis
3-post partum endometritis.

-↑ Risk for acquisition of HIV, herpes simplex virus type 2, gonorrhea, chlamydia & Trichomonas infections
18-how to treat gout in pt with CKD or if post transplantsteroid intracticular (best bc of lower S/E) if already on steroid post transplant then increase the dose.
19-when to treat bite wounds with primary closure and when to leave it openif high risk to infection no primary closure if not then suture.
1-Crush injuries
2-Bites on hands or feet
3-Wounds on body >12 hours or on face >24 hours
4-Cat bites (except on face)(dogs is not high risk)
5-Human bites (except on face)
6-Bite wounds in immunocompromised hosts.

face has a very good circulation and usually is not a high risk for infection.
20-wt is mc cause of bradycardia post mi and how to manage it-SAN is supplied with Right Coronary Artery(common with RCA ischemia)
-usually self-limited.
-if symptomatic cardiogenic shock (eg, hypotension, cold extremities, pulmonary edema), intravenous atropine is ttt
21-wt is pulmonary cachexia syndrome (PCS), wt cause, complications, and ttt?-loss of lean muscle mass associated with chronic lung disease (COPD).
-BMI <20 kg/m2 or weight loss >5% is suggestive
-occurs in 20-40% of COPD pts bc of increase work of breath(caloric use), systemic inflammation, muscle hypoxia, and steroid use.

-complications
1-impaired balance
2-increased susceptibility to lung infections
3-increased mortality.

-ttt:
-optimization of lung function
-exercise
-nutritional supplementation.
22- actinic keratosis has risk of SSC development, wt is the indication of biopsy? and how to treat if proven SSCBiopsy is indicated for AK when:
1-The diagnosis is unclear
2-Lesions >1 cm in diameter
3-Lesions are indurated
4-Ulceration is present
5-There is tenderness
6-Lesions are growing rapidly
7-Lesions fail to respond to appropriate therapy

-Biopsy-proven SCCs should be treated with either Mohs micrographic surgery or by an excision with 4 mm margins.
23- what is presbycusis-elderly gradually progressive SN hearing loss.
-initially affects the high-frequency range of hearing(obvious in a noisy, distracting environment).
-difficulties understanding rapid speech and a complex or less familiar vocabulary.
-speech discrimination test is normal, it will be abnormal after adding background noise.
24-infant botulism, cause, c/p, Dx, ttt and prognosis1-causes:
it happen after baby ingest C botulinum spors ( found in dust specially near construction sites or after earth quick, less common in honey) this bacteria colonize in baby GI (<1 year old, have less GI bacteria and commonly affected), then it will release toxin that block presynaptic cholinergic transmission.

2-C/P:
it is life threatening infection start as constipation and CN palsies (eg, ptosis, pupillary paralysis, weak suck, absent gag reflex) followed by progressive hypotonia and loss of deep-tendon reflexes(descending flaccid paralysis).

3-Dx by stool c botulinum spores or toxin.

4-ttt:
-must admit to ICU to monitor resp status
-NG tube feeding
-laxative medication
-physical and occupational therapies.
-IV human-derived botulism immune globulin (ASAP do not wait for confirmatory stool testing)

5-prognosis
-complete recovery if dx early and treated early.
-most infants will stay in ICU for 1-3 months may be longer if sever.
25-wt is the difference between infant botulism and foodborne botulism, and how does that change the managementinfant botulism happen after ingestion of spores and colonize the GI but foodborne botulism happen after infeston of preformed c boutulinum toxin.

treat infant one with human-derived botulism immune globulin
treat foodborne one with equine-derived botulism antitoxin.(It is usually avoided in infants due to the risk of severe anaphylactic reactions and lifelong hypersensitivity to equine antigens)
26-how to manage cystic lesion found incidentally in the pancreasit is either
1-pseudocysts
2-non-neoplastic
3-or neoplastic.

ultrasound guidance of the endoscope for needle biopsy
27- what are the stress testing factors associated with increase risk of cardiovascular event in the near future1-Clinical variables
-Poor exercise capacity
-Exercise-induced angina at low workload
-Fall in systolic blood pressure from baseline

2-ECG variables
->1 mm ST depression (flat or downsloping)
-ST depression at low workload
-ST elevation in leads without Q waves
-Ventricular arrhythmias

-if any present take to cath
-if negative (characterized by exertion to >85% of maximum HR with no significant ECG changes), denotes a <1% risk of cardiovascular events within the next year.
28-what is danger signs indicating a potentially life-threatening cause of headache1-Systemic symptoms (eg, fever) or illness (eg, cancer)
2-Neurological signs/symptoms
3-Onset is new
4-Other associated conditions (eg, head trauma)
5-Previous headaches with change in frequency, severity, or presentation
29-what is the first step in managing other wise health pt who is complaining of periodic headache-headache diary to record
1-triggers,
2-headache length,
3-associated symptoms
4-palliative techniques
-return for follow-up.
30-cluster headache c/p and ttt1-c/p
-affect M>F
-headaches that last <180 minutes and occur 1-8 times a day over a period of weeks.
-orbital, supraorbital, or temporal and always unilateral.
-restless agitation (unable to sit still)
-ipsilateral autonomic symptoms such as ptosis, miosis, lacrimation, conjunctival injection, rhinorrhea, and nasal congestion.
-can be so severe as to lead to suicide

2-TTT:
-if i acute active headache then give oxygen via mask (work 70%). if no relive then given intranasal sumatriptan in contralateral side of headache(not first line bc s/e is medication overuse headache), Intranasal lidocaine and ergot preparations are also sometimes used.
-for prevention in pt with >2 months use verpamil and some time we add topiramate (anticonvulsant)may be lithium or valportic acid.
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