nsuleman's version from 2018-01-13 05:46


Question Answer
what is Kartagener syndromeAutosomal recessive,It is a subgroup of a congenital mucociliary disorder known as primary ciliary dyskinesia. Consisting of:
1-situs inversus
2-chronic sinusitis
3-airway disease leading to bronchiectasis.
New York Heart Association heart failure classification-Class I: No symptomatic limitation of physical activity
-Class II Slight limitation of physical activity (eg, dyspnea with climbing stairs)
-Class III Marked limitation of physical activity (eg, dyspnea with house chores)
-Class IV Inability to perform physical activity without significant discomfort
Optimal medical therapy HF with left ventricular (LV) systolic dysfunction1-ACE inhibitor
2-beta blocker
3-loop diuretic
4-aldosterone antagonist.
Current guidelines recommend biventricular pacing devices for patients in sinus rhythm who meet all of the following criteria:1-LV ejection fraction <35% NYHA class II, III, or IV heart failure symptoms (essentially the presence of any symptoms)
2-Left bundle branch block with QRS duration >150 msec.
Indications for implantable cardioverter-defibrillator placement1-Primary prevention
-Prior myocardial infarction & LVEF ≤30%
-NYHA class II or III symptoms & LVEF ≤35%

2-Secondary prevention
-Prior VF or unstable VT without reversible cause
-Prior sustained VT with underlying cardiomyopathy.
how to verification a proper endotracheal tube (ETT) placement.1-normal capnogram has a characteristic rectangular waveform with 4 phases.

2- A colorimetric EtCO2 detector consists of litmus paper that changes color when exposed to CO2.
wt is intestinal helminths.Intestinal infection with Ascaris lumbricoides (roundworm), Trichuris trichiura (whipworm), and Ancylostoma duodenale (hookworm).

present in developing countries with poor water and sewage sanitation.
wt is Clinical manifestations of intestinal helminths(ascaris)reflect the life cycle of the infecting helminth with early, transient pulmonary symptoms (eg, dry cough, dyspnea) followed by long-term gastrointestinal symptoms (eg, nausea, vomiting, abdominal discomfort, diarrhea).
wt is work-up finding in intestinal helminths and how to treat itPeripheral eosinophilia is a defining feature, often have positive fecal occult blood. Diagnosis is usually confirmed with stool ova and parasite testing.

Treatment with oral albendazole is typically curative (mebendazole is slightly better for whipworm).
wt is the treatment of traveler diarrhea conditions1- intestinal helminths treat with albendazol 2- bacterial travelers' diarrhea treat with ciprofloxacin.
3- protozoal (giardia lamblia and entamoeba histolytica) treat with metronidazole.
4-enterotoxigenic E coli treat with TMX-SMX.
wt to follow closely after starting pt on TPNphosphate, bc dextrose will stimulate insulin that will drive pho intracellular to be used for oxifative phosphorylation.
wt is the complication of refeeding syndrome1-Seizures
3-Life-threatening cardiovascular complications (eg, arrhythmia, congestive heart failure).
wt is caput succedaneum(head swelling) in new born and how to manage them.Caput succedaneum is a scalp swelling above the periosteum that crosses suture lines, usually after prolong labor or assisted delivery. it is benign and resolve within first few days of life.
management of partial intestinal obstructionobservation and supportive treatment includes:
1-intravenous hydration
2-nasogastric suctioning
3-correction of electrolyte abnormalities
4-if fail to improve within 12-24 hours, early surgical intervention is recommended.
how to know if the intestinal obstruction is partial or complete if gas in the colon then it is partial.
Diverticular bleeding etiology Arterial erosion due to colonic mucosal outcropping
Diverticular bleeding c/p1-Painless hematochezia in patients age >40
2-Bleeding often self-limited but can recur. 3-Right side is more common than left side and may present with melena.
Diverticular bleeding/dx1-Colonoscopy
2-tagged red blood cell scan
Diverticular bleeding ttt1-Intravenous volume replacement
2-Endoscopic therapy or angiographic embolization
3-Colonic resection for persistent bleeding
how to differentiate tinea capitis hair loss from alopecia areatatinea capitis has scaling and inflammation in the area of hair loss.
wt is the most significant predictor of adverse cardiovascular outcomesDM
wt is the benefit of strict glycemic controlStrict glycemic control significantly lowers microvascular complications (eg, retinopathy, nephropathy, neuropathy) but does not consistently reduce macrovascular complications, eg, CHD, stroke
how to manage oral candidiasis 2/2 steroid INH1-insure proper inhaler use(if large amount of medicine stay in the mouth increase risk) 2-first treatment is topical as nystatin suspension or clotrimazole troches.
3- rinse mouth after using inhaler.
4- if topical fail then use oral fluconazole
when does hemochromatosis present (age)male present in fourth to sixth decade, female presnting later due to menstrual iron loss.
how to treat newly dx hemochromatosis therapeutic phlebotomy, with removal of approximately 1 unit of blood each week until iron stores normalize.
wt is common causes of acquired secondary hypogonadism1-use of anabolic steroids
2-chronic glucocorticoid
3-opioid use
5-chronic kidney or liver disease
7-pituitary tumors.
Wt is Enuresis and how to manage itdefined as urinary incontinence at age >5 and is most commonly due to primary nocturnal enuresis.

1-Urinalysis to rule out secondary causes
2-Lifestyle changes:
-Minimize fluid intake before bedtime
-Avoid sugary/caffeinated beverages
-Void before bedtime
-Institute reward system (eg, “gold star” chart)
-Enuresis alarm
3-Desmopressin therapy
what is c/p, dx/ttt of vasovagal syncope (neurocardiogenic syncope)1-Clinical presentation
-Inciting event (eg, emotional distress, painful stimuli, stress, prolonged standing)
-Prodrome (eg, pallor, nausea, diaphoresis) -Consciousness regained rapidly (eg, <1 minute)

-Mainly clinical diagnosis.
-Upright tilt-table testing in uncertain cases

-Avoidance of triggers
-Counterpressure techniques for recurrent episodes
how to manage vasovagal syncope (neurocardiogenic syncope)1-Education and reassurance.

2-Patients are advised to avoid triggers and assume supine position with raised legs at the onset of prodromal symptoms.

3- use physical counterpressure maneuvers (eg, leg crossing with tensing of muscles, tensing of arm muscles with clenched fists) to improve venous return and cardiac output, and abort an episode of neurocardiogenic syncope during the prodromal phase.
testicular torsion c/p, imaging, and management1-Epidemiology
-Most common in adolescents

2-Clinical features
-Testicular, inguinal, abdominal pain
-Nausea, vomiting
-Horizontal testicular lie with elevated testicle
-Absent cremasteric reflex
-Swollen, erythematous scrotum Imaging
-No blood flow on scrotal ultrasound with Doppler

-Surgical detorsion & fixation with exploration of the contralateral side
-Manual detorsion (if immediate surgery is not available)
wt is the best timing for surgical repair for testicular torsion-Detorsion within the first 6 hours typically allows for complete viability.
-After 24 hours, the testis is rarely salvageable.
how to manage insomnia first-line treatment for insomnia is Cognitive-behavioral therapy (CBT), if fail use hypnotic medications
wt is the most common side effect in elder who is taking hypnotic drugs that use for insomniaCommon adverse effects include daytime sedation, cognitive impairment, delirium, night wandering, agitation, balance problems, falls, and fractures and proven to increase mortality.
wt is Actinic keratosis (AK)is a pre-malignant condition caused by excessive sunlight (ultraviolet [UV] light) exposure. most commonly occurs in sun-exposed areas such as the face, scalp, ears, upper chest, and dorsal hands and forearms.
how does actinic keratosis present AK lesions are characterized by small, rough, erythematous, and keratotic papules that are often easier to feel than they are to see.
wt is the complication of actinic keratosis and how to manage itit increases the risk of squamous cell carcinoma. majority of SCC arise from pre-existing AK. so all AK should be removed, by
1-nitrogen cryosurgery
2-or by surgical excision or curettage.

Field therapy should be treated with 5-fluorouracil cream, topical diclofenac, imiquimod is recommended when numerous small lesions are present.
wt cause scabiesinfestation by the Sarcoptes scabiei mite, which burrows into the skin and spreads through direct person-to-person contact
how does scabies present Scabies usually presents with an intensely pruritic rash (often worse at night) in the flexor surfaces of the wrist, lateral surfaces of the fingers, and the finger webs. The rash is due to a delayed type IV hypersensitivity reaction to the mite (feces and ova included). can also involve other parts of the body (eg, elbows, axillary folds, nipples and areola in women, scrotum and penis in men)
how to dx scabies by physical and what testExamination usually shows excoriations with small, crusted, red papules scattered around the region, often with linear burrows. Patients can also develop small vesicles, pustules, wheals, and excoriations that can obscure the classic burrows in the skin.

Diagnosis is confirmed by skin scrapings from lesions revealing mites, ova, and feces under light microscopy.
how to diagnose tinea infection Potassium hydroxide staining of a skin sample
how does tinea present Tinea infections usually present as pruritic, erythematous, circular, and scaly lesions with central clearing.
wt is treatment of scabies1-eradicating the mites:
-by application of 5% permethrin cream over the whole body(excluding the head)then washing after 8-14 hours. S/E of this permethrin is local burning and pruritus.
-Oral ivermectin is also a treatment option, especially if difficult to use topical therapy or for outbreaks in nursing homes.

2-decreasing pruritus due to the dermatitis:
-Oral antihistamines
-topical steroids may be used for persistent dermatitis after mite eradication

3-prescribing oral antibiotics for any secondary bacterial skin infections.

4-All family members and close contacts should be treated to prevent re-infestation.

5-Bedding and clothing should be cleaned or placed in a plastic bag for at least 3 days as the mite can only live away from human skin for 2-3 days.
what is the first line pharmacotherapy for dementia-related cognitive impairment-Acetylcholinesterase inhibitors (eg, donepezil, rivastigmine, galantamine)
-NMDA receptor antagonist memantine is another medication
how to treat tention type headache1-Treatments with pharmacologic (eg, acetaminophen)
2-behavioral, or stress-reductive therapies are often helpful.
wt is Botulismserious presynaptic neuromuscular junction disorder caused by botulinum toxin produced by Clostridium botulinum (anaerobic organism), mainly after eating canned food. Botulinum toxin acts at peripheral nerve endings to inhibit release of acetylcholine into the synaptic cleft.
how does botulism present Botulinum toxicity leads ultimately to neuromuscular junction failure and subsequent weakness (limb and/or bulbar). It also leads to autonomic dysfunction (eg, blurry vision due to accommodation failure and impaired pupillary responses). Other botulism syndromes include infant botulism due to intestinal colonization, adult enteric botulism, and botulism associated with contaminated wounds.
how to dx botulismOn examination
1-sensory function is normal
2-multiple cranial nerve distributions may become weak
3-reflexes are usually diminished or absent.
4-Electromyography results may also suggest the diagnosis.

***confirmed by assay of the serum for botulinum toxin***
wt is myasthenia and how does it presentMyasthenia gravis (MG) is an autoimmune, postsynaptic, neuromuscular junction disorder caused by antibodies against the acetylcholine receptor.

It clinically presents with fatigable, fluctuating weakness (arms > legs), ptosis, diplopia, dysarthria, and dysphagia. Patients can develop purely bulbar variants of MG; however, autonomic dysfunction is rare and reflexes as well as sensory functions are usually normal.
wt is a major risk factor for patellar tendon tear use of fluoroquinolones
wt is physical exam and symptoms of patient with patellar tendon tear Immediate symptoms often include a "popping" sensation, pain, swelling, and difficulty bearing weight. Physical examination reveals swelling and tenderness in the anterior knee, often with superior displacement of the patella. With a complete tendon rupture, patients cannot actively extend the knee and cannot raise the leg against gravity.
wt does it mean when a patient present with symptoms suggestive of SAH and nerve III (CN III) palsy (ptosis and anisocoria)typical finding with posterior communicating artery aneurysms (about 20% of cerebral aneurysms) due to the proximity of the nerve to the artery's path. This finding can also be seen in cavernous-carotid aneurysms, but these are uncommon.
how does brainstem gliomas present Brainstem gliomas present with signs and symptoms of progressive brainstem involvement, including ataxia, cranial nerve palsies, and motor and/or sensory abnormalities.
how does posterior inferior cerbellar artery aneurysms present. How can you distinguish PICA (Wallenberg) from AICA?ataxia and bulbar dysfunction. PICA aneurysm affects the Nucleus ambiguous and nucleus solitarius with resultant loss of gag, taste, dysphagia, swallowing, etc This is only seen only in Wallenburg and not AICA aneurysm!!!
Motor involvement of the Trigeminal is seen only in lateral pontine (specially if it is a rostral lesion) with ipsilateral loss of touch and mastication on the side of the face
3.Facial involvement is sometimes seen in lateral pontine but not in lateral medullary syndrome with it's loss of anterior 2/3 taste, lacrimation, facial expression, corneal reflex, and hyperacusis