This generalized information is a limited summary of diagnosis, treatment, and/or medication

information. It is not meant to be comprehensive and should be used as a tool to help the user
understand and/or assess potential diagnostic and treatment options. It does NOT include all
information about conditions, treatments, medications, side effects, or risks that may apply to a specific
patient. It is not intended to be medical advice or a substitute for the medical advice, diagnosis, or
treatment of a health care provider based on the health care provider's examination and assessment of
a patient's specific and unique circumstances.

BEST OF LUCK

Prepared by : Dr Biruk Getachew W.

explanatory answers for COC MARCH 2020 , PART TWO of the booklet.
Components

1 emergency int med from 1 - 8

2 emergency surgery 9 - 16

3 emergency pedi 17 - 28

4 ENT 29-30

5 dental 31-36..

6 psychatry 37-44

7 optha 45-52
1 B , hmmm challenging to choose whether or not she has sever M , but the moral of the question
seems to be asking the firstline among the rx of sever malaria.

- all of the pts condition are in borderline to say sever.her RBS , her RR are in border line. The degree of
anemia is not mentioned. The parasite count along with the billurubin level is not mentioned as well.

Severe falciparum malaria: For epidemiological purposes, severe falciparum malaria is defined as one or
more of the following, occurring in the absence of an identified alternative cause and in the presence of
P. falciparum asexual parasitaemia.

Impaired consciousness: A Glasgow coma score < 11 in adults or a Blantyre coma score < 3 in children

Prostration: Generalized weakness so that the person is unable to sit, stand or walk without
assistance

Multiple convulsions: More than two episodes within 24 h

Acidosis: A base deficit of > 8 mEq/L or, if not available, a plasma bicarbonate level of < 15 mmol/L or
venous plasma lactate ≥ 5 mmol/L. Severe acidosis manifests clinically as respiratory distress (rapid,
deep, laboured breathing).

Hypoglycaemia: Blood or plasma glucose < 2.2 mmol/L (< 40 mg/dL

Severe malarial anaemia: Haemoglobin concentration ≤ 5 g/ dL or a haematocrit of ≤ 15% in children

< 12 years of age (< 7 g/dL and < 20%, respectively, in adults) with a parasite count > 10 000/µL

Renal impairment: Plasma or serum creatinine > 265 µmol/L (3 mg/dL) or blood urea > 20 mmol/L

Jaundice: Plasma or serum bilirubin > 50 µmol/L (3 mg/dL) with a parasite count > 100000/ µL

Pulmonary oedema: Radiologically confirmed or oxygen saturation < 92% on room air with a
respiratory rate > 30/ min, often with chest indrawing and crepitations on auscultation
 Significant bleeding: Including recurrent or prolonged bleeding from the nose, gums or venepuncture
sites; haematemesis or melaena

Shock: Compensated shock is defined as capillary refill ≥ 3 s or temperature gradient on leg (mid to
proximal limb), but no hypotension. Decompensated shock is defined as systolic blood pressure < 70
mm Hg in children or < 80 mmHg in adults, with evidence of impaired perfusion (cool peripheries or
prolonged capillary refill).

Hyperparasitaemia: P. falciparum parasitaemia > 2%

*Severe vivax and knowlesi malaria: defined as for falciparum malaria but with no parasite density

thresholds.

= Diagnosis of severe falciparum malaria

A correct diagnosis should be based upon a complete case history, a physical examination, and

laboratory investigations.

Both thick and thin blood films should be examined at health center or hospital level to demonstrate the
presence of P. falciparum asexual parasites.

However, it is important to note that:

Waiting for a blood smear result must not be allowed to delay the start of treatment unduly: if

clinical features strongly suggest severe falciparum malaria, treatment may be started before the results
are available.

Occasionally blood films may be negative even though the patient is suffering from severe

falciparum malaria. Following a negative result, blood films should be repeated, e.g. every 6

hours. Parenteral Artesunate may be initiated in such patients.

A positive blood film does not prove that severe falciparum malaria is the only cause of the

severe illness. Other possible causes should also be considered.

= mx of malaria ,

- sever falcipareum malaria : 1st line IV/IM artesunate -- 2nd line IM ARTHEMETHER ( iF ARTESUNATE IS
NOT AVAILABLE) - 3RD line quinine dihydrochloride : when parentral artesunate and arthemeter are not
available
- uncomplicated falciparum malaria : AL whether or not she is PX .. and add PQ to AL if pt is not px and
with out contraindication to PQ.

- Rx of uncomplicated malaria differs on d/t level of health facility and dependimg on specious

2D

- A - te pt is comatose , minimal parietal hemmorage by its own can not make pts comatose

- B : chronic , ere teww

- C : lacunar stroke : sx are usually focal , not generalized lile COMA in this pt.

Causes approximately 20% of all strokes; usually affects subcortical structures (basal

ganglia, thalamus, internal capsule, brainstem) and not the cerebral cortex.

Predisposing factor: A history of HTN is present in 80% to 90% of lacunar infarctions.

Diabetes is another important risk factor.

Narrowing of the arterial lumen is due to thickening of vessel wall (not by thrombosis).

The arteries affected include small branches of the MCA, the arteries that make up the

circle of Willis, and the basilar and vertebral arteries.

When these small vessels occlude, small infarcts result; when they heal, they are called

lacunes.

NB Lacunar stroke—Clinical features are focal and usually contralateral pure motor or pure

sensory deficits. Lacunar stroke includes four major syndromes:

o Pure motor lacunar stroke—if lesion involves the internal capsule.

o Pure sensory lacunar stroke—if lesion involves thethalamus.

o Ataxic hemiparesis—incoordination ipsilaterally.

o Clumsy hand dysarthria.

- D evidenced by , ,:this patient has sign of herination, defined by Cushing refoex triad , ( wide pulse
presurre : increasing SBP, decreasing DBP ), brady cardia , irregular respiration- Bradypnea usually,
tacchypnea may be
3 B

when approching a pt with coma, cheek for the pupils

- Pupils — The pupillary light reflex is tested in each eye individually to evaluate direct and consensual
responses. Disruption of the pupillary light reflex in comatose patients usually occurs because of either:

●Downward herniation of mesial temporal structures from an expanding supratentorial mass and/or a
lateral shift in the supratentorial compartment with stretching of the oculomotor nerve against the
clivus; or

●Primary brainstem lesions

In either of these, the third cranial nerves or their nuclei in the midbrain are injured, producing a
unilateral or bilateral oculomotor palsy. When unilateral, the ipsilateral pupil is dilated and unreactive
directly and consensually, but the contralateral pupil reacts to light shone in either eye. In some cases,
the pupil is dilated on the "wrong side," a phenomenon that is inadequately understood [8-10]. When
bilateral, there is neither a direct nor a consensual response, the pupils are symmetrically enlarged, and
the eyes are deviated outward.

In transtentorial herniation, after initial dilation and loss of light reactivity, pupils become somewhat
reduced in size (4 to 5 mm) and remain unreactive; they are called midposition and fixed. (See 'Coma
syndromes' below.)

Pupil size and symmetry should be noted as well. Pupils are normally between 3 to 7 mm in diameter
and equal, although approximately 20 percent of normal individuals have up to 1 mm difference in
pupillary size. Typically, the pupils are spared in metabolic and toxic conditions, except in certain toxic
syndromes, which are associated with either miosis or mydriasis

, hence option A & D are less likely

- this pt has normal V/S that rules out hypoperfusion as a cause.

4 B , asprin as one of the common cause of PUD and its compln.

5 D, we don see organ damage in this pt , that differenciate HTN urgency from Emergency ...

- #BG:

Causes approximately 20% of all strokes; usually affects subcortical structures (basal

ganglia, thalamus, internal capsule, brainstem) and not the cerebral cortex.

Predisposing factor: A history of HTN is present in 80% to 90% of lacunar infarctions.

Diabetes is another important risk factor.

Narrowing of the arterial lumen is due to thickening of vessel wall (not by thrombosis).

The arteries affected include small branches of the MCA, the arteries that make up the

circle of Willis, and the basilar and vertebral arteries.

When these small vessels occlude, small infarcts result; when they heal, they are called

lacunes.

A hypertensive emergency is the association of substantially elevated BP with acute

Hypertension Mediated Organ Damage (acute HMOD). Target organs include the retina,

brain, heart, large arteries, and the kidneys.

This situation requires rapid diagnostic workup and immediate BP reduction to avoid

progressive organ failure. Intravenous therapy is usually required. The choice of

antihypertensive treatment is predominantly determined by the type of organ damage.

Specific clinical presentations of hypertensive emergencies include:

o Malignant hypertension: Severe BP elevation (commonly >200/120 mm Hg)

associated with advanced bilateral retinopathy (hemorrhages, cotton wool spots,

papilledema).

o Hypertensive encephalopathy: Severe BP elevation associated with lethargy,

seizures, cortical blindness and coma in the absence of other explanations.

o Hypertensive thrombotic microangiopathy: Severe BP elevation associated with

hemolysis and thrombocytopenia in the absence of other causes and improvement

with BP-lowering therapy.

o Other presentations of hypertensive emergencies include severe BP elevation

associated with cerebral hemorrhage, acute stroke, acute coronary syndrome, cardio genic pulmonary
edema, aortic aneurysm/dissection, and severe preeclampsia and

eclampsia.
 Patients with substantially elevated BP who lack acute HMOD are not considered a

hypertensive emergency and can typically be treated with oral antihypertensive therapy

NB The clinical presentation of a hypertensive emergency can vary and is mainly

determined by the organ(s) acutely affected. There is no specific BP threshold to define

a hypertensive emergency.

6 B , precipitated by - the pt has "excessive urination" , note that Lasix precipitates HE in two ways :
Diuresis and Hypokalemia

Rate of fluid removal — The rate at which fluid can safely be removed in cirrhosis depends upon the
presence or absence of peripheral edema. When a diuresis is induced, the fluid is initially lost from the
vascular space; the ensuing fall in intravascular pressure allows the edema fluid to be mobilized to
replete the plasma volume. Fluid mobilization can be rapid (in some cases, exceeding 2 kg per day
without detectable intravascular volume depletion) in patients with peripheral edema .

By comparison, patients who only have ascites without edema can mobilize ascitic fluid solely via the
peritoneum. The maximum rate at which this can occur is only 300 to 500 mL per day; more rapid fluid
removal with diuretics (weight loss >0.75 kg per day)

Mean while , let us brief on hepatic encephalopathu :

- CATEGORIZATION AND GRADING

Hepatic encephalopathy is categorized based on four factors: the underlying disease, the severity of
manifestations, the time course, and whether precipitating factors are present (figure 1) [14-16].

●Underlying disease: A classification scheme based on the underlying disease has been proposed
[14,15]:

•Type A: hepatic encephalopathy occurring in the setting of acute liver failure

•Type B: hepatic encephalopathy occurring in the setting of portal-systemic bypass with no intrinsic
hepatocellular disease

•Type C: hepatic encephalopathy occurring in the setting of cirrhosis with portal hypertension or
systemic shunting
●Severity of manifestations: The severity of hepatic encephalopathy is graded based on the clinical
manifestations (table 1 and figure 2) [16] (see 'Clinical manifestations' below):

•Minimal: Abnormal results on psychometric or neurophysiological testing without clinical

manifestations (see 'Psychometric tests' below)

•Grade I: Changes in behavior, mild confusion, slurred speech, disordered sleep

•Grade II: Lethargy, moderate confusion

•Grade III: Marked confusion (stupor), incoherent speech, sleeping but arousable

•Grade IV: Coma, unresponsive to pain

7 D, pt seems to have aspiration pneumonia. Alcoholic - at risk for Aspiration pneumonia, plus Evidenced
by V/s derangement, febrile, sign complex of pneumonia. Elevated WBC. But the serum lipase level , and
84% spo2 are an entry point for dx of acute pancreatitis with ARDS ( abd pain vommiting , v/s
derangements ( SIRS) ) hence mechanical ventilation should be provided to treat the ARDS .

8 --- meningitis lemalet kehone , B... but still birth to indicate atypical preeclamsia as a DDX
lemaskemetm mokrewal

9 A , primary survey , ON ABCDE method , C is abnormal her, he is in shock but site is unknown,

B it is secondary survey

C he is anxious no more unconcious...

D CT for hemodynamically stable to look for z source of intraperitoneal bleeding

10 B , pt seem to have Rib fracture with emphysema. Rib fracture typically presents with pain on
inspiration associated with tenderness on palpation and sth subcutaneous crepitus.

- mx is primarly treating the pain on based on the pain score, although supplementing with o2 is part of
z supportive RX.

11 B, common causes of massive hemothorax include injury to lung parenchyma, intercostal

arteries( found both ant and posteriorly) or internal mamary artery ( found on aterior chest )

12 A

Treatment

Laparotomy remains the gold standard therapy for significant intra abdominal injuries. It is

definitive, rarely misses an injury, and allows for complete evaluation of the abdomen and

retroperitoneum

=.All patients with hypotension, abdominal wall disruption, or peritonitis

need surgical exploration. In addition, the presence of extraluminal, intra-abdominal, or

retroperitoneal air on plain radiograph or CT should prompt surgical exploration.

- Indications for Laparotomy

Blunt Penetrating

-Absolute Anterior abdominal injury with hypotension Injury to abdomen, back, and flank

with hypotension

- Abdominal wall disruption Abdominal tenderness

- Peritonitis GI evisceration

- Free air under diaphragm on chest radiograph

- High suspicion for trans abdominal trajectory after gunshot wound

- Positive FAST or DPL in hemodynamically unstable patient

- CT-diagnosed injury requiring surgery (i.e., ureter or pancreas)

- CT-diagnosed injury requiring surgery (i.e., pancreatic transection, duodenal rupture, diaphragm injury)

- Relative Positive FAST or DPL in hemodynamically stable patient

-Positive local wound exploration after stab wound

- Solid visceral injury in stable patient

- Hemoperitoneum on CT without clear source

B) Nonoperative Management of Blunt Trauma

The evolution of nonoperative therapy has been greatly advanced by the evolution of CT. CT

can not only make the diagnosis of solid visceral injury, but it can often rule out other

injuries requiring surgery. Solid visceral injuries can be graded as to severity.

13 i don see an indication here...

A- mx of basal skull # is generally conservative. indication for neurosurgical intervention for basal skull
fracture is when they have persisten csf leak for 7 days, then dural closure will be considered

B- altered mental status , her GCS is 12,

This pt had still GCS of 12/15 after 2 days of the insult. We don kw the background hx, that the pt may
had lucid interval in between. Normaly lucid interval of epidural hematoma lasts 24-48 hour, hence even
if this pt has Epidural hematoma, she is not a surgical candidate ( the only 3 indications for EDH is if pt is
detoriorating, or comatose gcs < 9 or , those with large bleed ;( > 30 cc or 1.5 cm thick , or midline shift >
5mm )

C depressed skull fracture ( is defined by inward displacement of a bome fragment, by atleast the
thickness of z skull - 2mm in temporal , 8 mm in parietal )

- DSF by it self is,not an indication for surgery but , is indicated in 3 condns,

- when - open depressed skull # or - in cosmotic area or - compression of large plate of bone > 1 cm )

d pneumocephalus : if ASXTIC - bed rest with 100% oxygen, to washout nitrogen and decrease
intracranial gar. : if SXTIC ( tention pneumocephalus - increased ICP ) : require neurosurgical
decompression

14 D from CT scan , he has Epidural hematoma. , though the Q is very vagure , option D is relatively the
answer because the pt seemingly had signs of increased ICP from midline shift ( elevated VBP, Pupillary
abnormality, even the pulse is near borderline) but to definately choose D as an answer, the significant
midline shift should have be mentioned

Acute Epidural hematoma: its natural hx is , usuall young age pt who sustained low energy trauma
usually 80% on temporal area, usually the bleeder is artery, the pt then will immediately loss
conciousness for 6-8hr , usually b/c of asstd concussion ( 1ry TBI) then 1/3 of pt will gain consciosness
and complain only headache +/- "sx complex of asst'd basal skull # ( if any) , then after 24-48 hr of lucid
interval, the hematoma expands and pt will again loss consciousness + rapid detorioration
follows( because artery is z bleeder) , with asstd contralateral hemiparesis , ipsilateral pupillary dilation
and cardinal sign of ICP

= CT lens shaped, biconvex hyperdense lesion

Mx : surgical : if detoriorating , or comatose < 9, or those with large bleed( 30 cc or 1.5 cm or midline
shift > 5 mm). conservative : otherwise if none of the 3 indications for surgery

Acute subdural hematoma : its natural hx is , any age , who sustained high energy trauma, hence will
have an associated 1ry TBI, hence LOC at presentstion that may detoriorate as the hematoma expands.
It can be. anywhere in the skull, usually the bleeder is vein, hence detoriorate slowly , 20-30% may
have lucid interval but it is not typical for it, and their lucid interval is a prolonged one. .

CT : diffuse concave hyperdense cresent shape ( lunate) b/C it can cross the suture line.
Hyperdense lesuon

MX : surgically if detorioration of GCS by >= 2 from time of injury to hospitalization, significant size > 1
cm , or significant midline shift > 5mm)

15 C , 75 MAP = 2* DBP +SBP /3

16 C

Anterior cord syndrome — The anterior cord syndrome is caused by direct or indirect injury to the
anterior spinal cord. Direct injury may occur secondary to a crush injury or compression from a
hematoma; indirect injury result from ischemia secondary to compression of the anterior spinal artery.
In athletes, anterior cord syndrome is typically seen after hyperflexion injuries with bony instability,
acute disc herniation, or hematoma formation.

The anterior cord syndrome, which involves injury to the spinothalamic tract, is characterized by loss of
motor, pain, light touch, and temperature sensation. Because the posterior columns are preserved, the
patient retains fine touch, vibration, pressure, and proprioception sensation distal to the injury.

Central cord syndrome — The central cord syndrome is the most common of the partial cord syndromes.
It is typically seen in older patients with degenerative spine disease and cervical spondylosis. In athletes,
the central cord syndrome is usually caused by hyperextension injury during which the ligamentum
flavum is thought to buckle, resulting in increased pressure on the central cord . It may also occur after
traumatic disc herniation, trivial trauma, or in hyperflexion injuries
The characteristic physical findings of central cord syndrome are bilateral motor paresis greater in the
upper than in the lower extremities, bladder dysfunction, and variable sensory loss below the level of
injury (figure 2). This pattern occurs because the most central portions of the spinal tracts contain fibers
from the upper extremities.

17 B

A May,be , especially excercise induced , but option B is more likely for the pts C/F and X ray .

Foriegn body aspiration :

More commonly, children with FBA present with partial airway obstruction. The most common
symptom is cough, followed by tachypnea and stridor, often with focal monophonic wheezing or
decreased air entry. Regional variation in aeration is an important clue to the diagnosis and is often
detected only if the clinician completes a thorough examination when the child is quiet and with
minimal ambient noise. Nonspecific findings of cough and generalized wheezing are often present. The
classic triad of wheeze, cough, and diminished breath sounds [30] is not universally present [11,30]. In a
review of 135 cases of airway FB in children, the classic triad was present in only 57 percent [11]. The
presence of the triad has high specificity (96 to 98 percent) for the diagnosis of FBA, but the sensitivity is
low

Imaging — For patients with suspected FBA who are asymptomatic, or symptomatic but stable, the first
step in the evaluation is to perform plain radiography of the chest. Subsequent steps depend on the
degree of clinical suspicion for FBA and may include CT or other modalities

Conventional radiography — Conventional ("plain") radiographic evaluation of the chest may or may not
be helpful in establishing the diagnosis of FBA, depending upon whether the object is radiopaque and
whether and to what degree airway obstruction is present. The diagnosis of FBA is easily established
with conventional radiographs when the object is radiopaque (approximately 10 percent of FBs).
However, most objects aspirated by children are radiolucent (eg, nuts, food particles) and are not
detected with conventional radiographs, unless aspiration is accompanied by airway obstruction or
other complications]. As a result, normal findings on radiography do not rule out FBA, and the clinical
history is the main determinant of whether to perform a bronchoscopy .. UPTODATE 2022

In children with lower airway FBA, the most common radiographic findings in lower airway FBA are ]:

●Hyperinflated lung (lucency distal to the obstruction) – This is caused by partial airway obstruction with
air trapping, such that air passes with inspiration but not with exhalation
●Atelectasis – This is usually caused by complete obstruction of an airway since air is resorbed from the
distal alveoli over time.

●Mediastinal shift – The mediastinum tends to shift away from the lung field containing the FB.

●Pneumonia – Infection often develops distal to an obstructed airway. Therefore, a consolidated

infiltrate is also a possible finding

Pulmonary abscesses and bronchiectasis are late manifestations of a retained airway FB

C ABRONCHIOLITIS typical age is infant and child less than 2 yrs

D CROUP Is,progressive plus rather stridor than wheeze

18 B

19 D

A & B- congenital heart ds and sepsis : no evidence for them

C Respiratory failure : plu edema is less likely because,he took approprate bolus dose of crystalloid fluid.

D 5 EPISODE OF VOMMITING OVER 12 HR too much to make z pt hypokalemic, unless replaced.

20 A amytryptaline is A TCA and has so many S/E

mx of TCA toxicity

- cardiac toxicity - wide QRS or ventricular arrythymia : NaHCO3 ( indian lecturers say " BI car beats Tri
car" )

- hypotention- NaHCO3

- TCA induced seizure : give benzodiazepine ( diazepam or lorazepam ) rather zan phenytoin.

- GI decontaminatiom : by charcoal

- refractory hypotention : if NaHCO3 fail , add IV fluid , if both fail, give epinephrine or phenylnephrine or
hypertonic 3% saline.
- refractory arrythymia : Mg or Lidocaine

21 B , this pt seem to have AFib from the ECG description, and the acute RX of AFib includes , rate
control , by BB ( metoprolo - the prefered l, propranol, esmolol )or CCB ( only use verapamil or diltiazim )
or Diagoxin ( 2nd line : prefered for pt with HF with reduced ejection fracture ) .

STG 4TH EDN .

Atrial fibrillation: is marked by disorganized, rapid, and irregular atrial activation which results

in irregular ventricular response. The ventricular rate is usually rapid. The ECG in Atrial

Fibrillation is characterized by the lack of P-waves, irregularly irregular ventricular response

and narrow QRS.

Atrial flutter: is characterized by regular rapid atrial rate of 260–300 beats per minute, which

usually results in a regular ventricular response in a 2:1 ratio resulting in a heart rate of 130–

150 beats per minute. The ventricular response can sometimes be in 3:1, 4:1, irregular or

rarely 1:1 ratio. The typical ECG finding is of saw-tooth appearance of the baseline mainly

on inferior leads (II, III, AVF) with rapid, regular and narrow QRS.

Treatment

The management of atrial fibrillation and atrial flutter are the same.

Objectives of treatment

Controlling ventricular rate

Prevention of thromboembolic events

Identification and treatment of the cause

Identification, prevention and treatment of precipitating factors

Non pharmacologic

Avoid stimulants (e.g., Caffeine, Khat) and alcohol intake.

Immediate electrical cardio-version-associated with hemodynamic instability (cardiogenic

shock) due to a rapid ventricular rate. If hypotension occurs at ventricular rate <130

beats/min, other causes of hypotension should be investigated. The energy requirement is

usually 100 to 200 joules; it should be synchronized.

Pharmacologic

Acute ventricular rate control

First line: Metoprolol, 2.5-5mg, IV, over 3–5 min, to maximum total dose 15mg over 10-15 minutes

Alternative

Digoxin, 0.25mg, IV, q2h until 1 mg total (digoxin is the first line medicine if atrial

fibrillation is associated with severe left Ventricular dysfunction)

Chronic ventricular rate control

First line:

Metoprolol, preferred beta blocker in patients with Heart Failure with depressed LV (left

ventricle) systolic function.

o Immediate release: 25-100 mg twice daily

o Extended release: 25-200mg/day

OR

Atenolol, 25-100mg P.O., daily

Alternatives

Digoxin 0.125 – 0.25mg P.O., daily. Digoxin can be added to beta blocker when the

ventricular rate control is suboptimal. It is the preferred agent when Heart Failure due to LV

systolic dysfunction is not well controlled.

OR

Verapamil, 40-80mg P.O., 2-3 times daily.

Anticoagulation to prevent cardioembolic cerebrovascular accident (CVA)

Risk stratifies patients for thrombotic complications with the CHA2DS2-VASc score
Summary :

There are two broad management issues that must be addressed early in patients with new

onset AF: the prevention of systemic embolization and the choice between a rhythm or rate

control strategy, both of which may improve symptoms.

Every patient with AF should be evaluated for the need of antithrombotic therapy to prevent

systemic embolization even for the first AF episode. This is accomplished by use of the

CHA2DS2-VASc score

Patients who require antithrombotic therapy include those in whom cardioversion (whether

electrically or pharmacologically) to sinus rhythm is being considered (regardless of the

CHA2DS2-VASc score or method of cardioversion [electrical or pharmacologic]) and those

who meet criteria for long-term anticoagulation. All patients whose risk of embolization

exceeds the risk of bleeding are candidates for long-term antithrombotic therapy.

Once ventricular rate control is achieved, a decision regarding the long-term management

(rhythm versus rate control) of AF should be made. A rhythm control strategy uses either

antiarrhythmic drug therapy, percutaneous catheter ablation, and/or a surgical procedure.

Electrical cardioversion may be necessary to restore sinus rhythm. Antiarrhythmic

medications are generally started before cardioversion and continued to maintain sinus

rhythm (in the event of AF recurrence).

A rate control strategy generally uses drugs that slow conduction across the atrioventricular

(AV) node, such as beta blockers, non-dihydropyridine calcium channel blockers, or digoxin.
ata suggest that rhythm and rate control strategies are associated with similar rates of

mortality and serious morbidity, such as embolic risk. However, there are several reasons why

pursuing a rhythm-control strategy would be preferred, including symptom improvement,

younger patient age, and irreversible structural and electrical remodeling that can occur with

longstanding persistent AF.

Beta blockers or verapamil or diltiazem are the preferred to digoxin in the absence of heart

failure (HF). Intravenous or oral amiodarone may help control rate when the other drugs are

ineffective or cannot be given. Digoxin is the preferred drug only in patients with AF and HF

with a reduced ejection fraction. Persistently increased ventricular rates in AF have been

associated with a left ventricular cardiomyopathy. this phenomenon is unlikely to occur if the

ventricular rate is kept below 110 beats/min, which is the recommended heart rate goal

In patients who are clinically or hemodynamically unstable (eg, myocardial ischemia,

pulmonary edema, hypotension) due to AF and a rapid ventricular response, treatment

options include intravenous rate control medications and/orimmediate cardioversion. In

patients with an adequate blood pressure, pharmacologic rate control with intravenous

calcium channel blockers or beta blockers may be attempted, while arrangements are made

for cardioversion

For the acute control of ventricular rate, intravenous beta blockade with metoprolol, propranolol, or
esmolol can be effective. Beta blockers may be particularly useful in states of high adrenergic tone (eg,
postoperative AF).

Suspected arrhythmia-induced cardiomyopathy are the same as those used in most other

patients with heart failure with reduced ejection fraction (eg, angiotensin converting enzyme

[ACE] inhibitors or angiotensin receptor blockers [ARBs], beta blockers, diuretics) and

tachyarrhythmias (eg, rate-control medications, consideration of antiarrhythmic

drugs and/or cardioversion

22 D , the pt collapsed after he already visited the triage, not he was found collapsed. Plus he has
palpitation with SOB, indicating circulatory cause is the insult. So i would say , D . Despite the Fact that
we follow ABC of life protocol ( which is recently revised as CAB of life in some text books )

23-27 : wereketu teftoal mesel

28 C , the phrase failure to passa 6f cathether , is entry point for dx of chonal atresia.

- CT with intranasal contrast or NASAL endoscopy are DXtic

-summary for choanal atresia.

CHOANAL ATRESIA : from UPTODATE 2022

Choanal atresia is obliteration or blockage of the posterior nasal aperture. Choanal atresia often is
associated with bony abnormalities of the pterygoid plates and midfacial growth abnormalities.

●Pathogenesis – One etiologic explanation for choanal atresia holds that persistence of the oronasal
membrane prevents the joining of the nose and oropharynx. This theory does not account for the
associated bony and midface abnormalities. An alternate explanation is that alterations in local growth
factors result in small or imperforate choanae [57]. Most cases involve bony and membranous
obstruction to varying degrees

●Incidence – Choanal atresia occurs in approximately 1 in 7000 live births [15]. It is more common in
girls than boys [21]. Approximately two-thirds of cases are unilateral [20,58].

●Presentation – The presentation of choanal atresia varies depending upon whether one or both sides
are involved. Individuals with unilateral choanal atresia typically present later in life with unilateral nasal
discharge and/or obstruction. Infants with bilateral choanal atresia typically present with upper airway
obstruction, noisy breathing, or cyanosis that worsens during feeding and improves when the infant
cries.

●Associated malformations and syndromes – Other congenital anomalies are present in 50 and 60
percent of individuals with unilateral and bilateral choanal atresia, respectively [20]. Choanal atresia
may occur as an isolated anomaly or as part of a multiple congenital anomaly syndrome (eg, Treacher
Collins, CHARGE [coloboma of the iris or choroid, heart defect, atresia of the choanae, retarded growth
and development, genitourinary abnormalities, and ear defects with associated deafness], Kallmann,
VACTERL/VATER association [vertebral anomalies, anal atresia, cardiac defects, tracheoesophageal
fistula and/or esophageal atresia, renal and radial anomalies, and limb defects], Pfeiffer) [59]. (See
"Syndromes with craniofacial abnormalities".)

Associated anomalies may include [15]:

•Facial, nasal, or palatal deformities

•Polydactylism

•Congenital heart disease

•Coloboma of the iris and retina (picture 8)

•Intellectual disability

•Malformations of the external ear

•Esophageal atresia

•Craniosynostosis

•Tracheoesophageal fistula

•Meningocele
●Evaluation and diagnosis – The diagnosis should be suspected if a number 5 or 6 French catheter
cannot be passed from the nose to oropharynx a distance of at least 32 mm [15]. Qualitative measure of
nasal airflow, such as the movement of a wisp of cotton under the nostrils or fogging of a mirror, adds
support to the clinical diagnosis [20]. Flexible or rigid nasal endoscopy can confirm the diagnosis by
demonstration of a narrow or absent opening from the nasal cavity into the nasopharynx (picture 9).

The diagnosis of choanal atresia is confirmed by computed tomography with intranasal contrast that
shows narrowing of the posterior nasal cavity at the level of the pterygoid plate (image 6).

In addition to a thorough physical examination to detect associated anomalies, cardiology and

ophthalmology consultation are warranted for infants with choanal atresia.

●Management – Immediate management of infants with bilateral choanal atresia includes placement of
an oral airway and initiation of gavage feedings [15].

Definitive repair involves transnasal puncture and stenting (picture 10) or endoscopic resection of the
posterior nasal septum through a transnasal approach with or without stenting (picture 9) [60,61]. The
transnasal puncture alone has fallen out of favor because of an unacceptable rate of recurrence [20,58].
Advantages of the transnasal endoscopic approach include clear vision of the operative field and
accurate removal of the atretic plate and posterior vomerine bone without damage to surrounding
structures [62]. The classic transpalatal approach is reserved for difficult or recurrent cases (picture 11).
Recurrent stenosis may occur even after successful surgery

29 A , this pt seems to have either laryngeal CA or Apical lung CA, cus he is old pt, smoker , with
progressive and or persistent horseness of seversl months . Even though apical lung CA as well can cause
horseness of voice, top in z list , laryngeal CA is z most likely. And intial imaging for laryngeal CA is
CT/MRI ( accordong to STG 4th edn, ) , PET with CT (according to uptodate 2022) , so yegnaw sewech
new tyakewn yawetut bemilew , i would go for A,

30 A, swelling of floor of mouth, carious lower 2nd molar teeth , are an entry poing for ludwings angina.
Which is commonly known as cellulitis of floor of the mouth. What might be against in this question is
the relatively longer day of presentation ( 5 dsy )
Summary of ludwimgs angina.

Ludwig angina is a bilateral infection of the floor of the mouth that consists of three compartments: the
submandibular, sublingual, and submental spaces

udwig angina is characteristically an aggressive, rapidly spreading "woody" or brawny cellulitis involving
the bilateral submandibular, sublingual, and submental spaces. The infection most commonly arises
from an infected second or third mandibular molar tooth. Ludwig angina is characterized by its lack of
lymphadenopathy and abscess formation.

Over two-thirds of patients with Ludwig angina have a dental source of infection, usually involving the
second or third mandibular molar teeth

Other sources of infection include contiguous spread from peritonsillar abscess or suppurative parotitis,
trauma to the mandible or floor of the mouth, and sialolithiasis and infection of the submandibular or
sublingual salivary glands

ce established, infection evolves rapidly. The tongue may enlarge to two or three times its normal size
and distend posteriorly into the hypopharynx, superiorly against the palate, and anteriorly protruding
out of the mouth, causing a “double-tongue” appearance [5]. Immediate posterior extension of the
process will directly involve the epiglottis

MICROBIOLOGY

Ludwig angina is typically a polymicrobial infection involving flora of the oral cavity The most common
organisms isolated from deep neck space infections are viridans streptococci, reflecting their abundance
in the mouth.

CLINICAL FEATURES
Patients typically present with fever, chills, and malaise, as well as mouth pain, stiff neck, drooling, and
dysphagia, and may lean forward to maximize the airway diameter [12]. They may have a muffled (“hot-
potato”) voice or be unable to speak at all. Trismus is usually absent initially unless there is spread into
the parapharyngeal space. As the illness progresses, breathing may become difficult; stridor and
cyanosis are considered ominous signs

DIAGNOSIS

The diagnosis of Ludwig angina is established based on the presence of suggestive clinical findings (see
'Clinical features' above), usually with the support of imaging studies.

Diagnostic imaging — Computed tomography (CT) of the neck with intravenous contrast is the imaging
modality of choice for the diagnosis of Ludwig angina and other deep neck space infections

TREATMENT

The treatment of Ludwig angina involves timely assessment and management of the airway and empiric
broad-spectrum antibiotics ,,,,, While maintenance of an adequate airway is the primary concern and
may necessitate urgent tracheostomy. most cases can be managed initially by close observation and
intravenous antibiotics. If cellulitis and swelling continue to advance or if dyspnea occurs, artificial
airway control should be gained immediately, before the onset of stridor, cyanosis, and asphyxia.

-Surgery directed to the infected region is not usually necessary since it is uncommon to have a
drainable collection in the early stages of infection. Surgical drainage is important if abscesses are
identified by imaging. Similarly, if infected teeth are identified as the cause, these should be addressed
after appropriate consultation.

31 B ,

Pulpitis — Pulpitis, inflammation of the dental pulp, occurs when progression of dental caries exposes
the dental pulp, leading to infection. The early and dominant symptom of acute pulpitis is a severe
toothache that can be elicited by thermal changes, especially cold drinks.

Pulpitis can be classified as reversible or irreversible. Reversible pulpitis occurs when caries encroach on
the pulp and is associated with mild inflammation of the pulp. Irreversible pulpitis refers to ongoing
inflammation within the pulp chamber with rapid buildup of pressure, occlusion of blood vessels at the
apical foramen, ischemia, and necrosis of the pulp tissue.

Irreversible pulpitis is characterized by acute and intense pain and is one of the most frequent reasons
that patients seek emergency dental care. Apart from removal of the tooth, the customary approach to
relieving the pain of irreversible pulpitis is by drilling into the tooth, removing the inflamed pulp (nerve),
and cleaning the root canal. A minority of dentists begins with a trial of antibiotics and analgesics,
although there is no proof of benefit from this approach.

32 B, "Apart from removal of the tooth, the customary approach to relieving the pain of irreversible
pulpitis is by drilling into the tooth, removing the inflamed pulp (nerve), and cleaning the root canal. "
uptodate 2022

33 A , Pericoronitis —evidenced by the involvement of the unerupted wisdom teeth gingival flap,
commonly in masticator area, with limited opening the jaw in this pt.

Pericoronitis is an acute localized infection caused by food particles and microorganisms trapped under
the gum flaps . The infection involves the wisdom teeth in adolescents and adults, and occurs during the
eruption of the permanent teeth in children. The major symptoms include pain and limitation of
movement on opening the jaw, discomfort on mastication and swallowing, and facial swelling.

The pericoronal tissues are erythematous and swollen, and digital pressure can often express an
exudate from under the infected flap. The masticator spaces are often involved, which can produce
trismus. Localized painful lymphadenopathy may be noted, and the breath is usually foul.

34) B/C( because securing airway is done after watching for the pt for some time) but , more likely B ,,
obviously this pt has ludwings angina ( infection of all the 3 spaces ) and its mx as mentioned above is ,:-

TREATMENT

The treatment of Ludwig angina involves timely assessment and management of the airway and empiric
broad-spectrum antibiotics ,,,,, While maintenance of an adequate airway is the primary concern and
may necessitate urgent tracheostomy. most cases can be managed initially by close observation and
intravenous antibiotics. If cellulitis and swelling continue to advance or if dyspnea occurs, artificial
airway control should be gained immediately, before the onset of stridor, cyanosis, and asphyxia.

-Surgery directed to the infected region is not usually necessary since it is uncommon to have a
drainable collection in the early stages of infection. Surgical drainage is important if abscesses are
identified by imaging. Similarly, if infected teeth are identified as the cause, these should be addressed
after appropriate consultation.

NB, the choice of ABX for IMmuno competent, Immunocompromized is D/T.

- immunocompetent :

* ampicil - sulbactam or Ceftra ... plus ... metro

* if cant take pencillin/cephalospir : levoflox plus metro or ertapenem alone.

- immuno compromi

* cefepime plus metro plus vanco/linezolid

Or

* meropenem plus vanco/linezolid

Or

* piperacillin tazobactam plus vanco/linezolid

35 - so vast to revise

36 A ,

Differentials for benign cystic lesions of jaw , when ever asked for such topics, remember the F.F ...

1 radicular cyst : asst'd with non viable tooth , 52.2 %

2 most periodental cyst ( lateral , apical, residual) : anywhere in oral cavity with vital tooth

3 dentigerous ( follicular cyst ) - can be coronal, lateral, cirrumfrential : impacted , 3rd molar , canine, &
premolar teeth

4 Premordial : mandibular 3rd teeth

5 static bone cavity : below inferior alveolar canal

************ PSYCHATRY section ********

before answering the FF questions... challneging psychatric questions needs 2 things, 1 focus on the
duration of symptoms, 2 the chronology of symptos. so let us clear the high yiepd psychatric terms.
Psychatric illness are for this disscussion purpose, catagorized into 6 class ( 1 schizophernia spectrum &
other Psychotic D/O, 2 MOOD d/O - Depression, bipolar mnamn 3 disorders of emotions : anxiety
phobia panic , 4 personality D/O 5 childhood D/O : ADHD, conduct D/O etc. 6 Somatic symptom &
related disoreder ( somatic sx disoreder, illness anxiety disoreder, conversion disoreder, etc )

1 ) schizophernia spectrum and other psychotic D/O : include Schizophrenia and its Differential other
psychotic disorders ( isolated delutional DO, brief psyhotic D/O, schizophreniform DO, schizoaffective
D/O, schizotypal personality D/O( this one is special case among the DDX) , substance & medical related
psychotic DO, catatonia D/O due to another medical condn)

- let us first define Psychosis before we Brief z defn of all the above DDX

Psychosis is a break with reality with delusions, hallucinations, disorganized or illogical

thinking, and chaotic behavior. Although psychosis is a hallmark of schizophrenia, it is not

pathognomonic for the disorder.

1.1 Schizophrenia : is a chronic psychosis defined be the presense 2 of the following 5 domains of
psychosis ,

- delusion - hallucination - incohorent spech or illogicallity - bizzare behavior ( odd or disorganized acts
endemalet new ) - catatonia.

Among this, schizophernia lemalet chronic ( > 6 mo) of atleast 2 of the above sxs is needed, and of the 2 ,
one should be either delusion or hallucination.

- now let us see the DDX for schizophrenia : these DDX ke schizophrenia , differe by either duration or by
having additional SX from other class of major class of disordered mentioned above , or by having lesser
number of SX that they do not fullfill for schizophernia.

1.2 Brief PSychotic Disorder : they full full the SXtic criteria of schizophernia but the duration is > one
day & < 1 month. Duration of an episode of the disturbance is at least a day but less than a month, with
eventual full return to premorbid level of functioning.

1.3 schizophreniform disorder : they fullfill the sxtic criteria of schizophrenia but the duration is > 1
month & <6 month

1.4 delutional disorder : unlike schizophernia they have only delusion, but none of the other 4 optional
components of schizophernia ( if any, they will be brief, non prominet, or have direct relation to the
delusion ( for ex , delusion of infestation sinorachew, they may have an associated tactile hallucination -
sensation of being infested woth insects ) , PLUS atleast duration of 1 month is enough to dx delusional
DO.

1.5 Schizoaffective Disorder : like schizophernia , they meet the sxtic criteria for schizophernia( i could
not find source for the defn of the duration ) , but additionaly they meet the criteria for major
depressive disoreder , or manic episode or mixed episode.

= surprisingly , unlike the name of the disorder, the psychatric symptoms ( the sxs of schizophernia )
lasts for short time & these symptoms of schizophenia , like delusion &/or hallucination intially happen
for usually the first 2 weeks without significant mood sx, but then , the mood Symptoms ( depression,
mania , or mixed ) willl come and must be present for significant portion of the duration of the active
peroid of the illness.
1.6 major depressieve or Bipolar disorder with Psychotic features.

= these pts have the defn fullfilled for sx and duration of MDD or BPD, but they also have psychotic
component ( delution /or hallucination /or catatonia ) that may or may not fullfill defn of schizophernia.

=to differentiate from schizoaffective D/o : unlike SA-DO :- 1 , they may not fullfill criteria fir
schizophernia 2 the above mentioned typical chronology of sxs of SA-DO aynorm.

= to differentiate MDD /BPD with psychotic feature vs Schizophernia : The former pts, in between acute
episodes of their mood swing, they become very normal , plus psychatric symptoms are congrunt to the
mood symptoms ( ድ ባ ቴ ላ ይ ያ ለ ሰ ው , የ ማል ረ ባ ነ ኝ ብ ሎ ሲ ያ ስ ብ - delusion of inadequacy,
nehillistic delution ነ ው የ ሚኖ ራ ቸ ው : ,BUT schizophernia pts dont get complety normal in between
episodes. And they are usually incongrunt to the mood ( የ ሚያ ሳ ዝ ን ነ ገ ር እ ያ ወ ሩ ይ ስ ቃ ሉ ).

1.7 substance induced psychotic d/o : they will have obvious HX of abuse of substances

1.8 psychotic D/O 2ndry to General medical condn : they will have obvious history of chronic diseases
like CLD CKD vascualr disease - SLE , stroke, etc...

1.9 OCD : ይ ች ን የ ማያ ቅ የ ለ ም መቸ ስ

1.10 PTSD : ይ ች ን ም , bayhon the duration should be 1 month , yemilew endayresa.

2 MOOD disoreders : has 2 components

= A (( : Bipolar & related disoreder ( includes Bipolar 1 disorder , bipolar 2 disoreder, cyclothymic
disorder, substance/medication induced BPD , ETC ))

= B (( : depressive & related disorders ( includes MDD- single episode , MDD - recurrent episode ,
persistent DD { dysthymia } , Disruptive mood dysregulation disoreder, substance/medication induced
DD, premenstrual Dysphoric disoreder, unspecified DD, other specified DD ))

2.1 Bipolar disorders : also called manic - depressive disoreder. hence the prefix " BI- Polar"

2..1.1 Bipolar 1 disorder : is characterized by atleast 1 lifetime or more manic episodes or mixed ( both
manic and depressive sx at a time ) episodes , that is/are usually preceded by major depressive episodes.

NB Criteria for manic episode : a distinictive peroid of abnormally and persistently elevated expensive or
irritable mood and abnormaly & perisistently elevated goal directed activity or energy lasting atleast 1
week ( usually it lasts 3-6 momth) , and these sxs should present most of the hour of the day & nearly
every day . but note that,some times the duration for the defn can be any duration ( even hours of
manic symptoms, if hospitalization is mandated) .
= during this high energy manic mood disturbance , atleast 3 or more among the following 7 noticable
changes should be there

1 inflated self estemm or even delution of grandiosity

2 decreased need for sleep ( unilke insomina, they dont even want to sleep - እ ኔ እ ኮ ብ ዙ
የ ምሰ ራ ው ስ ራ አ ለ ብ ኝ ነ ው የ ሚሉ ት ።

3 more talkative than usuall or pressure to keep talking

4 flights of ideas or subjective experience that thoughs are racing

5 distractablity ( their attention is easly drawn to unimmportant or irrelevant external stimulus )

6 increase in goal directed activities or psychomotor agitation ( purpose less non goal directed
activity )

7 excessive involvement of activities that have a high potential for painfull consequences likr foolish
business involvement, engaging in unrestrained buying spees, sexual indissection.

NB2 CRITERIA for MAJOR DEPRESSIVE DISORDER episodes : on the way of defining major depressive
episodes let us brief major depressive disoreder.

2.1.2 Bipolar 2 disorders : has one or more major depressive episodes with atleast one HYPO manic
episodes.

= How to differentiat BP1D/O from BP2D/O : BP1 D/O - they have mania ,not hypomania plus they sth
may not have a precceding Major depressive symptoms. But BP2 D/O must have one or more major
depressive episodes and have atleast one episode of HYPOmania, not mania.

= how to d/ciate hypomania from mania :- hypomanic episodes are characterized by changes in mood ,
energy , activity , behavior , and cognition, that are similar to those of mania , but less sever. Like 1
mood can be elevatedd or euphoric but commonly they rather experince irritablity, dysphoric than
euphoric. 2 self estem may be inflated but never reach point of delutiinal grandiosity that occur in mania
3 thinking of hypomanic pts are quick and more of goal directed unlike manic pts whose thoughts are
racing disconnected and lead to aimless ineffective activities 4 hypomanic speechs are loud and rapid
but are easier to interupt than manic speech

5 risk taking behavior in hypomanis is mild to moderate but manics have sever 6 by defn ,
hypomanic pts dont have asstd psychotic symptoms , and dont need hospitalization , unlike manic pts.

2.1.3 cyclothymic disorder : these pts will have hypomania and mild depression cycling every 2 year.

2.2 MAJOR depression disorder

- it is usually recurrent, but fewer pts may have only 1 episode

- DX requires the ff sx and duration : 1 or major depressive episodes , each lasting 2 or more weeks ( in
most hours of the day, and all days of the weeks) , and the sxs of MD epsiodes are defined by presence
of 5 or more of the following 9 sxs , Abbrevated as " A SAD FACES " - A for anhedonia- loss of interest in
activities or reduced ablity to find pleasure in normally enjoyable experiences., S for sleep abnormality A
for appetite abnormality D for dysphoria -decreased mood ( feeling unhappy dissatisfaction or
frustration ) F for fatique A for agitation C for concentratiom loss, E for esteem - low S for Sucide idea
or attempt

37 C , panic attack is the single event that has both cognitive and somatic behavioral component, but
panic disorder is a DXtic term.

3 . Anxiety Disorders, PTSD and OCD

There are different types of anxiety disorders:

Specific Phobia – At least 6 months of irrational and persistent fear and marked

avoidance of a specific thing, place or circumstance, to the extent that it interferes

with normal functioning.

Social Phobia – At least 6 months of noticeable and persistent fear of being

negatively evaluated for at least one social or performance situation.

Panic Disorder– At least one panic attack (acute episode of unprovoked, intense

fear/distress accompanied by somatic or cognitive symptoms) resulting in worry

about having another panic attack.

NB Panic disorder — Panic attacks may occur in both panic disorder and specific phobia. To differentiate
these disorders it is helpful to consider the context of the panic attack. Panic disorder is characterized by
uncued or unexpected panic attacks, whereas panic attacks within the context of specific phobia are
typically cued by encountering the feared situation or stimulus

Generalized Anxiety Disorder (GAD) – At least 6 months of excessive and

uncontrollable daily worry about multiple themes (e.g., school, family safety, world

issues, natural calamities, friends, personal performance) that results in physical

symptoms and functional impairment.

OCD and PTSD are not considered as anxiety disorder according to DSM 5

Post-Traumatic Stress Disorder (PTSD) – Following an exposure to significant

trauma avoidance or re-experiencing of the trauma for at least one month as

illustrated by: intense fear, disturbing dreams, flashbacks, helplessness,

physiological agitation upon seeing reminders of the event, or disorganized/agitated

behavior.

Obsessive-Compulsive Disorder (OCD) – recurrent, intrusive, inappropriate and

unwanted thoughts, or images, causing significant anxiety that interfere with usual

functioning.

Agoraphobia — Multiple specific phobias may resemble agoraphobia. To distinguish these disorders,
consider the focus of fear in the situation. In specific phobia, the focus of fear is on aspects of a
particular situation, so multiple specific phobias will be associated with multiple fears (eg, driving is
avoided for fear of an accident; elevators are avoided for fear of being stuck; outdoor places are avoided
for fear of spiders). In agoraphobia, avoidance is typically across a range of situations, yet the focus of
fear is the same across situations (eg, driving, elevators, and outdoor places are avoided for fear of panic
symptoms or the unavailability of help if needed)

38 D , because this pt has the following highlighted features

= let us define peripartum onset defn of DSM5 : The DSM-5 specifier “with peripartum onset” is used
when onset of major depression occurs either during pregnancy or in the four weeks following delivery.

= let us first see , the DSM5 cruteria for MDD

Depressive symptoms

≥5 symptoms during the same two week period that are a change from previous functioning; depressed
mood and/or loss of interest/pleasure must be present; exclude symptoms clearly attributable to
another medical condition
Depressed mood

Most of the day, nearly every day; may be subjective (e.g. feels sad, empty, hopeless) or observed by
others (e.g. appears tearful); in children and adolescents, can be irritable mood

Loss of interest/pleasure

Markedly diminished interest/pleasure in all (or almost all) activities most of the day, nearly every day;
may be subjective or observed by others

Weight loss or gain

Significant weight loss (without dieting) or gain (change of >5% body weight in a month), or decrease or
increase in appetite nearly every day; in children, may be failure to gain weight as expected

Insomnia or hypersomnia

Nearly every day

Psychomotor agitation or retardation

Nearly every day and observable by others (not merely subjectively restless or slow)

Fatigue Or loss of energy, nearly every day

Feeling worthless or excessive/inappropriate guilt

Nearly every day; guilt may be delusional; not merely self reproach or guilt about being sick

Decreased concentration

Nearly every day; may be indecisiveness; may be subjective or observed by others

Thoughts of death/suicide

Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without specific plan, or
suicide attempt, or a specific plan for suicide

Additional required criteria

Must have all 4, plus ≥5 depressive symptoms above

Symptoms cause clinically significant distress or impairment in social, occupational, or other important
areas of functioning
Episode not attributable to physiological effects of a substance or another medical condition

Episode not better explained by schizoaffective disorder, schizophrenia, schizophreniform disorder,

delusional disorder, or other specified and unspecified schizophrenia spectrum and other psychotic
disorders

No history of manic or hypomanic episode

Exclusion does not apply if all manic-like or hypomanic-like episodes are substance-induced or are
attributable to physiological effects of another medical condition

************ ******** ********

The differential diagnosis of postpartum unipolar depression includes normal postpartum-related

changes, postpartum blues, and bipolar depression, as well as other psychiatric disorders

Normal postpartum changes — The somatic symptoms of major depression (changes in sleep, energy
level, and appetite) overlap with changes observed in postpartum women who are not depressed.
Clinicians can determine whether problems with sleep, energy, and appetite are due to depression or to
normal puerperal-related changes by evaluating these symptoms in the context of normal expectations
for the puerperium.

Postpartum blues — Depressive symptoms such as dysphoria, insomnia, fatigue, and impaired
concentration can appear in both postpartum major depression and postpartum blues. However, the
two disorders are distinguished in that the diagnosis of postpartum blues does not require a minimum
number of symptoms. In addition, the symptoms of postpartum blues are mild and self-limited;
symptoms typically develop within two to three days of delivery, peak over the next few days, and
resolve within two weeks of onset. By contrast, the diagnosis of major depression requires a minimum
of five symptoms that must be present for at least two weeks Symptoms of postpartum blues that
persist beyond two weeks are best viewed as postpartum depression rather than postpartum blues.

Bipolar depression — Postpartum depression can represent bipolar depression rather than unipolar
depression [163,164]. As an example, in a prospective study of postpartum women who screened
positive for depression (n = 826), the primary diagnosis was unipolar depression in 69 percent and
bipolar depression in 23 percent [111].
Bipolar depression is marked by a past history of hypomania (table 3) and/or mania (table 4). Also,
agitation may be more prevalent in bipolar depression. In one prospective study of women diagnosed
with bipolar major depression (n = 180) or unipolar major depression (n = 547), agitation was reported
more often by women with bipolar depression than unipolar depression . Additional information about
distinguishing bipolar major depression from unipolar major depression is discussed separately.

Other psychiatric disorders — Other psychiatric disorders (eg, psychotic disorders) that are part of the
differential diagnosis for postpartum major depression are discussed elsewhere, in the context of
nonperinatal major depression.

MINOR DEPRESSION

Unipolar minor depression is diagnosed in patients with two to four depressive symptoms lasting for a
period of at least two weeks, and no history of mania or hypomania

39 D , because he has only manic episode that lasted a week he fulfill BP 1 disorder, but we cant choose
A, that need atleast 1 Major Depressive episode to dx.

40 A , these pt has criteria for MDD and the rx options are Fluoxetiene, sertaline or 2ndline
amytryptaline. So option A,C,D are possible answers. But the side effects mentioned like dry mouth ,
constipation, and blurring of vision are commonly implicated for Tricyclic anti depressants
( amytryptalline, amoxapine, desipramine, Doxepin, imipramine) because they affect reuptake of not
only serotonin but also Nor epinephrin in the presynaptic terminal. Hence exposing these drugs to be
metabolized by the enzymes in the synapse and make them unavailable for the next neuronal fire from
presynaptic channel. Hence the above side effects are due to malfunctioning of the peripheral
sympatatic nervious system.

41 C ,

A- even though the duration goes for it, the pt should have been fully return to premorbid level of
functioning. But the phrase "Relatively well" does not go will fully ( absolutely well ).

B- emmm may be , but the delution should be isolated( if not, asstd sxts should be subtle) , but this pt
has significantly symptomatic disorganized speech too.

C- more likely dx... long standing delution ( because it says he has been, not he had been ) plus
disorganized speech... fullfilles the criteria for schizophernia.

D- the duration, he had the Sxs for the last 5 years, even though he was relatively well untill last 2 days

42 C , obviously, plus 1 yr duration.

43 D ,

Mx of alcohol intoxification and withdrawal

Intoxication = naloxone (IM/IV) 0.04-15mg mg; if there is no response, the dose should be

increased every 2 minutes

Withdrawal = Pharmacological Treatment: thiamine (IM) 300mg 24 hourly. For the CNS symptoms.
diazepam (PO) 10 mg every 4–6 hours on the first 24 and reduce by 20% over 5 days (only in inpatient
care) OR Lorazepam

Delirium Tremens = diazepam (IV)10mg for immediate sedative or hypnotic action. If no response gives
a second dose. OR lorazepam (IM/IV) 2mg for immediate sedative or hypnotic action. If no response
gives a second dose. OR chlordiazepoxide (IV) 20–60mg taper over one month AND thiamine (IM) 100-
300mg 24hourly OR vitamin B Complex (IV) 1ampoule in 500ml 5% Dextrose.

44 A.

= the phrase " she appears to be indifferent ( having no particular interest ) indicate that it is not somatic
sx disoreder, because this,pts have persistent thought or anxiety abt their symptoms.

DDX

1 conversion disorder

Diagnostic and Statistical Manual, Fifth Edition (DSM-5) — A DSM-5 diagnosis of conversion disorder
requires each of the following criteria

●One or more symptoms of altered voluntary motor or sensory function

●Clinical findings that demonstrate incompatibility between the symptom and recognized neurologic or
general medical conditions (eg, Hoover's sign of functional limb weakness or a positive entrainment test
for functional tremor)

●The symptom or deficit is not better explained by another medical or mental disorder
●The symptom or deficit causes significant distress, psychosocial impairment, or warrants medical
evaluation

The diagnosis rests upon positive clinical findings that indicate the symptom is incongruent with
anatomy, physiology, or known diseases, or is inconsistent at different times (eg, a “paralyzed” limb will
move inadvertently when the patient is distracted by performing movements in their unaffected limb)
[1]. However, normal findings on physical examination (eg, reflexes) or normal laboratory tests do not
constitute “positive clinical findings.”

DSM-5 describes several subtypes of conversion disorder that are based upon the presenting symptom
or deficit [1]:

●Seizures or attacks – These events are also called psychogenic nonepileptic seizures, and are marked
by abnormal generalized limb shaking and apparent impaired or loss of consciousness resembling
epileptic attacks or fainting (syncope)

●Weakness or paralysis

●Abnormal movement – Includes dystonic movement, gait disorder, myoclonus, and tremor

●Anesthesia or sensory loss – Includes symptoms such as loss of touch or pain sensation

●Special sensory symptom – Includes visual (eg, double vision, blindness, or tubular visual field [tunnel
vision]), hearing (eg, deafness), or olfactory disturbance

●Swallowing symptom – This symptom is also called globus sensation or globus pharyngeus and is
characterized by the sensation of a lump in the throat (see "Globus sensation")

●Speech symptom – Includes dysphonia and slurred speech

●Mixed symptoms – Two or three different subtypes of symptoms are present (eg, paralysis plus
blindness)

2 Somatic symptom disorder is usually diagnosed in general medical settings based upon a history,
physical and mental status examination, and laboratory tests.

Diagnostic criteria — We recommend that somatic symptom disorder be diagnosed according to the
DSM-5; the diagnosis requires each of the following

●One or more somatic symptoms that cause distress or psychosocial impairment.

●Excessive thoughts, feelings, or behaviors associated with the somatic symptoms, as demonstrated by
one or more of the following:

•Persistent thoughts about the seriousness of the symptoms

•Persistent, severe anxiety about the symptoms or one’s general health

•The time and energy devoted to the symptoms or health concerns is excessive

●Although the specific somatic symptom(s) may change, the disorder is persistent (usually more than six
months).

In addition, DSM-5 includes several specifiers (qualifiers) for making a more precise diagnosis
●With predominant pain – The predominant somatic symptom is pain.

●Current severity – With regard to excessive thoughts, feelings, and behaviors, how many of these three
features are present. The number of somatic symptoms is also used to determine severity:

•Mild – Only one feature is present (eg, excessive time and energy devoted to somatic symptom).

•Moderate – Two or more of the features are present (eg, both persistent thoughts and severe anxiety).

•Severe – Two or more of the features are present, plus the patient manifests either multiple somatic
complaints (eg, fatigue, dizziness, and gastrointestinal distress) or one very severe somatic symptom.

●Persistent – The course of illness lasts more than six months, psychosocial functioning is markedly
impaired, and the current severity is rated as severe.

45 B, the pt obviously has gravis Ds, its opthalmic festures are exopthalmus, lid lag lid retractdion and
so on..

46 D, she has malignant hypertention , which is Malignant hypertension: Severe BP elevation

(commonly >200/120 mm Hg)

associated with advanced bilateral retinopathy (hemorrhages, cotton wool spots,

papilledema).

The clinical presentation of a hypertensive emergency can vary and is mainly

determined by the organ(s) acutely affected. There is no specific BP threshold to define

a hypertensive emergency.

Mx of Malignant hypertension with or without thrombotic microangiopathy or acute renal failure

 timeline and target BP is reducing the BP over Several hours by , , MAP −20% to −25%by Labetalo
as firstline or Hydralazine as second lime.

TREATMENT of Increased ICP ,

The treatment of increased intracranial pressure is specific to the underlying etiology.

VISUAL PROGNOSIS

Permanent loss of vision is a common consequence of papilledema that is untreated or unresponsive to

treatment. Clinical findings predictive of visual loss are high-grade disc edema, peripapillary subretinal
hemorrhages, opticociliary shunt vessels, abnormal vision at presentation, and the development of
visual field loss. Anemia, old age, myopia, glaucoma, and systemic hypertension have been found to be
risk factors for a poor prognosis in some studies [60]. Progressive changes in the visual field or acuity are
useful to predict patients at risk; however, vision loss sometimes occurs abruptly. Visual field loss
attributed to hemorrhage can be expected to resolve.

47 A both CN3 and CN4 and occulo sympathethic nurve seems to be affected ,

-horner syndrome is paresis of the occulosympathetic nerve which normaly function to dilate pupil,
superior tarsal muscle which help to elevate eyelid, sweat secretion in the face , hence its palsy causes,
triad,of meosis, partial ptosis, and anhydrosis.

- D was supposed to be the likely answer, but , occulomotor nerve ,CN3 , has 3 functions ;

- controlong the 4 out of 6 muscles ( except lateral rectus , and superior oblique, that is why ,pt with CN3
palsy have outward and down ward displacement of the eye because of counter functining of lateral
rectus ( CN6 ) and superior obliques muslce innervated by CN4 ) . but in this question it says" he has
limitation of movement of the eye in all direction except abduction. Hence these pt has not only CN3
plasy but also CN4 ( superior obliques ) palsy. plus to choose D, pt should have mydratic pupil.

- supplies the upper eye lid muscle hence its palsy will fail to elevate the eyelid

- supplies parasympatatic innervation for pupil constriction. Hence its palsy causes , mydriasis

Triad of mydriasis + strabismus of the 4 affected directions + ptosis suggests pure CN3 palsy

48 B, KOH ena Fungus ayfatum a. Plus she aquired it from leaf of plant
49 A , " whitish dandruff like scales, normal mebomiam gland , scalp lesiom goes for seborrhoic.

B-

c- louse infestation , in hair of scalp and eye lash binor noro

D has,isolated eye lesion

50 B,

Disorders of eyelash

1 trichiasis : downward misdirected eyelash caused by chemical burn , glucoma, sataph blepheritis , HZ
virus, bla bal... and if untreated it will cause trauma to cornea, hence opacity.

2 trichomegally : significant elongated eyelash caused by malnutrition, porphyria, hypothyrodsm

2 poliosis : premature whitening pigmentation of eyelid , caused by vitiligo, tuberous sclerosis, marfan
syndrome, etc

3 mederosis : spontaneous loss of eye lash