MEDICINE MCQ REVIEW 2012 AL COLOMBO

(YEAR 2019)

1. Drugs with survival benefit in cardiac failure

a. Digoxin F
b. Ivabradine T
c. Frusemide F
d. Carvedilol T
e. Spironolactone T

Drug Mortality Mechanism of Other trial examples

benefit action important
Spironolactone present reverse the effects 1.Risk of hyper RALES trial
of aldosterone kalemia
stimulated by 2.If K > 5
compensatory don’t give
mechanisms 3.Monitor SE
while on this
4.SE - painful
gynaecomastia
Beta blockers present Inhibit Several large Carvedilol,
sympathetic clinical trials metoprolol,
activity bisoprolol
might reduce the
risk of disease
progression in
heart failure,
improve
symptoms and
increase survival.
ACE inhibitors present 1.reduce after SE – cough , V-Heft II captopril,
load by angioedema , trial Enalapril
reducing first dose
vasoconstriction hypotension
1. When
by AT 2 , and by
giving ACEI
increasing
check SCr if
bradykinin patient has RAS
which is a , SCr will rise
vasodilator 2. When
giving ACEI

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 2.reduce pre check K risk
load by of
reducing Na and hyperkalemia
water retention 3. ARB
only given if
by reducing
ACEI
aldosterone
intolerance, CI
or as a second
3.prevents line drug
cardiac
remodeling

Ivabradine present binds to funny 1.Risk of

channel , reduce I bradycardia
current , reduce 2.If HR > 70
the slope of with beta
depolarization, blocker 
inhibit sinus node added on to it

Furosemide absent symptomatic No trials-

benefit only. withholding
furosemide is
not possible
and not
ethical.
nitrates absent Reduce the V HeFT I
duration of trial
hospital stay. ( nitrates +
Hydralazine)
digoxin absent improves Dig trial
contractility of
the heart ,
prolongs the
refractory
period of AV
node , increase
vagal tone
-

02. Thrombocytopenia occurs in

a. Chronic liver cell disease T

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b. Hemophilia A F
c. SLE T
d. Leptospirosis
e. Polycythemia rubra vera T

Decreased production-drugs, toxins,

Vitamin B12/folate deficiency, Bone marrow
failure –aplastic anaemia, myelofibrosis,
Bone marrow infiltration –leukaemia,
Platlet disorders
metastases

Bone marrow infiltration-Immune

reduced number- thrombocytopenia (ITP),DIC/TTP,Viral
THROMBOCYTOPENIA infections/Bacterial infections, Increased
destruction

Sequestration-Hypersplenism

acquired- Drugs. Aspirin, clopidogrel, High

blood urea, High doses of garlic, Eosinophilia

Reduced function-
THROMBASTHENIA
inherited- vwf

A. CLCD people have get thrombocytopenia by hypersplenism, bone marrow suppression,

decreased hemopoietin growth factors, increased destruction, alcoholism and other multiple
pathways.
B. Hemophilia A is factor viii deficiency. In platelet function disorders namely VWf disease
they get platelet disorder functional factor viii deficiency both because platelets have a
receptor to transport factor viii. But in Hemophilia the deficiency is only factor viii and no
associated thrombocytopenia.
C. SLE cause a pancytopenia
D. Blood parameters in Leptospirosis- platelet reduced, mild to moderate anemia, Neutrophil
leukocytosis with only marginal white cell elevation but leukopenia also possible.
E. In polycythemia rubra vera RBC, WBC and platelets are increased.

03. Renal diseases correctly matched with the cause

a. Membranous nephropathy – bronchial CA T

b. Acute interstitial nephritis – ibuprofen treatment T
c. Acute tubular necrosis – low dose aspirin
d. Acute cortical necrosis – Russel’s viper T

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e. Chronic interstitial nephritis – metformin F

04. In the management of cardiac failure, influencing renin angiotensin

aldosterone system,

a. Is done by the use of ramipril T

b. …………………………
c. Improves remodeling of heart F
d. Should be considered in all patients T
e. Is indefinitely used in patients with left ventricular failure

a. This is an ACEI. Same efficacy as enalapril at equivalent doses.

b. ………………………………….
c. Mechanism of action of ACEI
o 1.reduce after load by reducing vasoconstriction
by AT 2 , and by increasing bradykinin which is a vasodilator
o 2.reduce pre load by reducing Na and water retention by reducing aldosterone
o 3.prevents cardiac remodeling

d. This is a first line drug. Should considered in all. ARB s are given only to those intolerable for
ACEI.
e.

05. Advantages of LMWH over unfractionated heparin

a. No need of monitoring T
b. Effect is easily reversible F
c. Due to its long half life, it doesn't have to be given as an infusion T

d. Less heparin induced thrombocytopenia T

e. Can be managed as outpatient T

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06. Regarding giant cell arteritis

a. Is a large vessel vasculitis - F

b. Visual loss is a complication - T

c. Is treated with high dose steroids -T

d. Is associated with polymyalgia rheumatica -T

e. ESR is < 50mm/ 1st hour in majority-F

Answer:

Giant cell arteritis (GCA) and polymyalgia rheumatica (PMR) are related diseases associated with a
granulomatous arteritis of medium-sized vessels of the head and neck.

The cardinal symptom of GCA is headache, which is often localized to the temporal or occipital region
and may be accompanied by scalp tenderness. Jaw pain develops in some patients, brought on by
chewing or talking, and due to ischemia of the masseter muscles. Visual disturbance can occur and a
catastrophic presentation is blindness in one eye due to occlusion of the posterior ciliary artery. On
fundoscopy the optic disc may appear pale and swollen with hemorrhages, but these changes may take
24–36 hours to develop and the fundi may initially appear normal. Other visual symptoms include loss
of visual acuity, reduced color perception and papillary defects. Rarely, neurological involvement may
occur, with transient ischemic attacks, brain-stem infarcts and hemiparesis

Ix- The typical laboratory abnormality is an elevated ESR, often with a normochromic, normocytic
anaemia. CRP may also be elevated and in some cases this precedes elevation of the ESR. (The ESR
usually exceeds 50 mm/h and may exceed 100 mm/h- Medscape)

Mx- Corticosteroids are the treatment of choice and should be commenced urgently in suspected GCA
because of the risk of visual loss (Box 25.76). Response to treatment is dramatic, such that symptoms
will have completely resolved within 48–72 hours of starting corticosteroid therapy .

If there are no symptoms or signs of visual loss, initial treatment with the equivalent of prednisone 1
mg/kg (maximum 60 mg/day) administered in a single daily dose Davidson’s 21st Edition

Threatened or established visual loss at diagnosis ,intravenous "pulses" of methylprednisolone,

customarily administered as 500 to 1000 mg intravenously each day for three days, followed by oral
therapy with prednisone 1 mg/kg/day (maximum of 60 mg/day) ~Up-to-date

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07. Regarding erysipelas

a. Edges are discrete and merge into the skin -F

b. Caused mainly by group A beta hemolytic streptococci- T
c. Affect dermis and superficial subcutaneous tissue- T
d. Systemic spread can cause multi organ dysfunction- some case reports online
e. Penicillin are the treatment of choice -T

Answer:

Erysipelas is a more superficial involvement of the subcutaneous tissue and lower dermis. The most
common organism causing both Cellulitis and Erysipelas is group A Streptococcus. Erysipelas has a
characteristic raised erythematous edge, indicating involvement of the dermis. It usually affects the face
or the legs, while cellulitis most commonly involves the legs. Blistering occurs in both conditions.

Rx- Treatment is with an antistreptococcal agent such as phenoxymethylpenicillin, or in cases of

penicillin sensitivity, erythromycin or ciprofloxacin. In severe cases, intravenous antibiotics are
indicated ~Davidsons 21st Edition

(The duration of therapy should be individualized depending on clinical response; 5 to 14 days is usually
appropriate~ Up-to-date )

08. Regarding pneumonia

a. ………………………..

b. Erythromycin is an alternative for doxycycline in atypical pneumonia-T

c. Treatment with ciprofloxacin delays the diagnosis of tuberculosis-T

d. Cough persisting without fever is an indication to change the antibiotics- F

e. Chest radiography features resolve before the resolution of clinical symptoms- F

Answer:

all hospitalized patients with CAP are treated with a regimen that includes coverage for atypical
pathogens because pneumonia caused by atypical pathogens can be severe and cannot be clearly
distinguished from other types of pneumonia at the time of diagnosis.

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b)In the treatment of mycoplasma pneumonia, antimicrobials against M pneumonia are bacteriostatic,
not bactericidal. Tetracycline and erythromycin compounds are very effective. The second-generation
tetracyclines (doxycycline) and macrolides are the drugs of choice Medscape

c)Empiric use of fluoroquinolones should not be used for patients at risk for M. tuberculosis without an
appropriate assessment for tuberculosis infection. The administration of a fluoroquinolone in patients
with tuberculosis has been associated with a delay in diagnosis, increase in resistance, and poor
outcomes~UpToDate

d & e)Clinical response to therapy — With appropriate antibiotic therapy, some improvement in the
patient's clinical course is usually seen within 48 to 72 hours (table 6). Patients who do not demonstrate
some clinical improvement within 72 hours are considered non responders

09. Prolonged use of inhaled corticosteroids cause

a. Hoarseness of voice-T

b. Fetal growth restriction-F

c. Oropharyngeal candidiasis-T

d. Diabetes mellitus-F

e. Sleep disturbances- No clear link established

Answer:

EFFECTS OF LOCAL DEPOSITION:

● Dysphonia (hoarse voice) is a common complaint among users of inhaled glucocorticoids

(ICS).

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 ● Oropharyngeal candidiasis (thrush) may be a problem in some patients, particularly elderly
patients, patients taking concomitant oral glucocorticoids or antibiotics, and patients inhaling
glucocorticoids at high dose or more often than twice daily

● Allergic contact dermatitis has occasionally been described due to ICS, particularly budesonide
● Other — Cough and throat irritation, sometimes accompanied by reflex bronchoconstriction,
may occur when ICS are given via MDIs.

Randomized trials have not shown a connection between use of inhaled corticosteroids (ICS) and risk
for diabetes; however, these studies might have been underpowered to detect this association
(https://www.jwatch.org/jw201101110000002/2011/01/11/inhaled-corticosteroids-might-provoke-
diabetes)

SYSTEMIC ADVERSE EFFECTS

risk of developing adverse systemic effects from ICS is influenced by several factors, including the dose
delivered to the patient, the site of delivery (ie, mouth, lungs, gastrointestinal tract), the delivery system
used, individual differences in the response to the glucocorticoid, and individual comorbidities

● Adrenal suppression — Systemic administration of glucocorticoids causes hypothalamic-

pituitary-adrenal (HPA) axis suppression by reducing corticotrophin (ACTH) production,
which reduces cortisol secretion by the adrenal gland
● increased intraocular pressure and increased risk of cataract formation
● growth deceleration in children and increased risk for osteoporosis in both adults and children.
● Osteoporosis and fracture risk in adults
● Skin changes and bruising
● Myopathy

(UpToDate)

10. Hyponatremia is a feature of

a. Adrenal failure-T

b. Decompensated cirrhosis- T

c. Treatment with metformin- F

d. SIADH-T

e. Thiazide diuretics-T

Answer:

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11. Regarding scrub typhus

a) T - CNS involvement can occur in severe forms of the disease.

b) F – Scrub typhus by orrientia. Prowaleski transmits epidemic typhus.
c) T – finding the eschar in physical examination is useful for the diagnosis. However it is not found in
every instance.
d) F – No such prophylactic methods have been identified so far. But Doxy is used in the treatment.
e) T – severe infection can cause a vasculitis. This can give rise to thrombocytopenia and with a PUO.

12.Regarding tuberculosis

a) F – BCG vaccination doesn’t prevent any infection. It only serves as a means to limit CNS and
disseminated TB involvement.
b) F – Smear negative Pulmonary TB and Extra pulmonary TB have no bacilli in the sputum.
c) No question.
d) T / F ? – Should be for more than 9 months, but cant say a duration for sure. Better to leave.
e) T – A special form exists in the ward for TB notification.

13. Postural hypotension is a feature of

a) T – a recognized complication of Addison’s disease.

b) T – a side effect of the drug.
c) T – A known case due to dehydration by Diuretic overuse. Specially in elderly.
d) F – Gives rise to hypertension. Mostly episodic spells of hypertensive symptoms.
e) F – Gives rise to secondary hypertension. As in Cushing’s disease.

14. Regarding a lesion in the posterior column

a) No Stem.
b) T – Posterior columns carry fibers to the same side. Therefore ipsilateral loss.
c) F – No motor fibers carried.
d) T – Reflexes below the lesion are lost.
e) T – Known to occur in sensory ataxia with posterior column involvement. ( Syphilis, B12 deficiency)

15. Which of the following are true regarding X linked dominant

Diseases

a) F – affected males are severe than female heterozygotes. Females have 2 X chromosomes, hence
lionization can occur to inactivate one, unlike in males.
b) F – Only Y chromosome transfers from father to son. Hence, no male to male transmission.
c) Unsure. Mostly consanguinity affects autosomal recessive disorders.
d) F – Females transmit to Females too. Mothers X chromosome goes to daughters and son as well.
e) F – Transmits to 50% of offspring.

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Single Best Response

26) In general Cushing due to ectopic ACTH secreting tumor shows metabolic changes rather than other
typical features of Cushing disease or disease.
Those metabolic changes are
 Hypokalemia
 Metabolic Alkalosis
 Pigmentation
The common and the best answer would be Hypokalemia. Hyponatremia is not a feature of Cushing.

27) Here they are asking for the test to diagnose the condition there fore with the history we need to
come to a probable diagnosis and do the relevant test. Just doing blood culture wont relieve a bacterial
infection and a diagnosis.
History is somewhat towards the dengue but this is not common scenario for dengue since it is 2 days
history of fever without other typical features like arthralgia myalgia and headache and it is same for
the leptospirosis as well.
Malaria explains the scenario fully and this is showing hemolytic anaemia and liver involvement. So
the answer is Malaria with the strong travel history .
As there is no organomegaly rash or involvement of GI tract typhoid is unlikely.
Even for the typhoid there are no organomegaly and eschar.

28)

Acute exacerbation of asthma usually not presents with chest pain if it is not exacerbated by LRTI where
patient can have localized pleuritic type chest pain and also there won’t be this type of ECG changes in
acute exacerbation. Even though he is known asthmatic scenario is not compatible with asthma.
It is same for the COPD as well and if it is complicated with cor pulmonale there are ECG changes like
P pulmonale that is high amplitude of P wave in aVf v2 and v3.
For the answer C Inversion of T can be the Ischemic changes but they are not the typical ECG changes.
And there no risk factors in the history as well.

Myocarditis is an inflammatory disease of the myocardium with a wide range of clinical presentations,
Patients with myocarditis may present with the following signs and symptoms:
 Mild symptoms of chest pain (in concurrent pericarditis), fever, sweats, chills, dyspnea
 In viral myocarditis: Recent history (≤1-2 wks.) of flulike symptoms of fevers, arthralgia, and
malaise or pharyngitis, tonsillitis, or upper respiratory tract infection
 Palpitations, syncope, or sudden cardiac death due to underlying ventricular arrhythmias or
atrioventricular block (especially in giant cell myocarditis)
 Heart failure
Investigations
 Complete blood count (CBC) - Leukocytosis (may demonstrate eosinophilia)
 Elevated erythrocyte sedimentation rate (and other acute phase reactants, such as C-
reactive protein)
 Rheumatologic screening - To rule out systemic inflammatory diseases

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  Elevated cardiac enzymes - Creatine kinase or cardiac troponins
 Serum viral antibody titers - For viral myocarditis
 ECG - Electrocardiograms are often nonspecific (e.g., sinus tachycardia, nonspecific ST-
or T-wave changes

ACS also can present with this picture but here there is no other autonomic symptoms
like sweating and vomiting and the pain is not typical. Other parameters like tachycardia
and pressure value can be there. Cough is no a typical feature anyway. If the patient has
developed acute heart failure there can be cough as well due to pulmonary edema.

All of this explain the pulmonary embolism with history of travel in a flight. Other
symptoms you can work out and ECG changes due to RV strain.

29)

Here is the next step should be CBS or NCCT brain which is not there. If we take this as a
stroke due to ischemia the answer is IV tissue plasminogen activator.

30)

The answer is perianal fistula.

Pan colitis is a feature of UC where as crohns affect from mouth to anus. Both perianal fistula
and abscess are feature of Crohn`s disease. But out of them fistulae are the commonest where
as causes for perianal abscess in general are idiopathic mainly then DM and then crohn`s.

Calprotectin can be elevated in both infection and inflammation as well lactoferrin.

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 And both have the positive family histories.

31. b Acute glomerular nephritis

AGN- classical presentation >hematuria, oliguria, hypertension, edema.

UFR- RBC and RBC casts, granular cast(RBC ,WBC casts..), sub nephrotic range
proteinuria (<3.5g/d, <4+)
s.Cr is elevated(normal range 0.6-1.2)
Acute interstitial nephritis (increased s.cr, eosinophilia and eosinophiluria ,UFR- RBC, WBC ( RBC
cast can present but not common), classical triad of fever ,rash and eosinophilia with hx drug intake)

32. d) 95% chance that the population mean will fall within the confidence interval

33. Acute Pericarditis- ECG changes- saddle shape(concave) ST elevation in all leads. T inversion.
(Constrictive pericarditis- low voltage QRS complexes.)
Myocarditis- ST and T changes with arrhythmias.
Other Causes for ST elevation – MI,L Ventricular aneurism, hyperkaliemia, brugada syndrome

34 a. Anti-mitochondrial antibody.
This is the clinical and biochemical presentation of primary biliary cholangitis. Immunologically
mediated Progressive destruction of bile ducts. Common in women and majority aged 40-50.
Pruritus is a early feature and subsequently jaundice developed.
AMA are positive in almost all patient and elevated ALP is the often liver biochemistry abnormality.

35. a USS KUB

No need of further evaluation if the first episode of uncomplicated uti in healthy young men. Here,
considering age should do further assessments. So best next investigation is USS KUB as it is easily
available, inexpensive and safe. Can evaluate bladder lesions, prostate, kidney and upper and lower
ureters.

36. 20 year old previously healthy female presenting to hospital eight hours after ingesting an
unknown number of paracetamol tablets. what is the next best management option?
a. gastric lavage following NAC
b. N acetyl cysteine
c. active charcoal
d. methionine
e. wait for one more hour and do according to nomogram
answer is b
has to start NAC without waiting for blood levels as amount is unknown.
 Emesis, activated charcoal if within 1 hr
 Oral methionine if within 12 h and not vomiting
 May not be effective if activated charcoal has been given already
 IV N-acetylcysteine (loading 🡪 maintenance)
 If NAC is started, continue until prothrombin time starts to improve
 Liver failure sets in after about 36 hours
 If suspected, prophylactic liver failure regimen is started
 Liver tests normalize within 1 week (biopsy abnormal up to 3 months)

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  Paracetamol does not cause CNS depression until hepatic encephalopathy sets in hence if
drowsy earlier on, suspect concurrent overdose with other drugs
NAC 150mg/kg in 5%glucose over 15-60min
50mg/kg in 500ml 5%glucose over 4 hours
100mg/kg in 1000ml 5%glucose over 16 hours
Ongoing mx- do INR, U&E, LFT. IF INR rising continue NAC until <1.4
17.45 year old drug user presenting with intermittent fever and a murmur on left lower sternal
edge diagnosed to have infective endocarditis. Most probable causative organism
a. streptococcus epidermidis
b. streptococcus bovis
c. streptococcus viridans
d. pseudomonas aeruginosa
e. staphylococcus aureus
answer is e
staphureus cause infective endocarditis in previously normal tricuspid valve specially in
intravenous drug users.
Causes-strep viridans commonest followed by staphaureus,strep bovis(colon cancer patient),
enterococci, coxiella burnett
Prosthetic valves-staphylococcus epidermidis
Rarely HACEK gram –ves,chlamydia,fungi
Other-SLE(libman sack endocarditis), malignancy
Clinical- fever,malaise,night sweats,new or change in murmur,LVF(Aortic root abcess causing
regurgitation)
IMMUNE phenomenon-ROSI
EMBOLIC phenomenon-abcesses,janeway lesions,
Diagnosis-modified dukes( cultures,echo)
RX- antibiotics- penicillin(vancomycin)+gentamycin for 4-6 weeks
Surgery if- HF,valve destruction,repeated emboli,fungal IE, large abcess

18. 15-year-old girl presenting with past history of intermittent jaundice for last few years.
Investigations are as follows.
Hb – 13.2
WBC – 6.3, N – 62%, L – 34%
Platelets – 282
LDH – 200
Direct bilirubin – 6
Indirect bilirubin – 34
AST – 14
ALT – 26
INR – 1.2
ALP – 140
GGT – 25
Most likely diagnosis?
a. Gilbert syndrome
b. Biliary atresia
c. Dubbin Johnson syndrome
d. Cholecystitis

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e. Rotor syndrome
answer is a
total bilirubin 40 and direct is less than 2o% so its indirect bilirubinemia.
Indirect causes-hemolytic anemia,gilbert xd( deficiency of udp glucoronyl transferase)
Direct- obstruction to enter canaliculi-dubin jhonson,rotors
Obstructed internal biliary system-alagille, biliary atresia
Obstructed external biliary system-biliary atresia,choledochal
cyst,stones,malignancy,strictures

19. 18-year-old school boy present with one day history of reduced urine output. He is previously
healthy and is a long-distance runner.
BU – 10
Serum creatinine – 900
Na – 132
K–6
Possible etiology for his renal failure?
a. CKD
b. Dehydration leading to hypotension
c. Interstitial nephritis
d. Rhabdomyolysis
e. ……………………………
scr is out of proportion to BU. So dehydration unlikely. rhabdomyolysis with long running is
possibility!!!

20. A patient presenting 4 hours after ingestion of an organophosphate. BP – 80/50, PR – 56, RR

– 23, SpO2 – 88%. On auscultation crackles were heard. Next most appropriate step of
management?
a. 250ml 0.9% NaCl
b. Nebulize with salbutamol
c. Oxygen via venturi mask
d. Atropine 3mg IV bolus
e. Pralidoxime 1g IV over 30 minutes
next most appropriate is the atropine 2mg IV every 10min upto full atropinization(skin dry,
pulse>70,pupils dilated).

41. D

The ECG changes correlate with a true posterior MI which shows reciprocal changes which are ST
depression in leads V1–V3 with a dominant R wave, and ST elevation in lead V5/V6

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Postero-lateral MI will have ST elevation in the lateral leads and reciprocal changes in V1 and V2

Myocarditis presents with fatigue, dyspnea, palpitations. In the Physical examination soft heart sounds
may be heard, with a prominent third sound and often a tachycardia. A pericardial friction rub may also
be heard

Brugada syndrome is an inherited condition and has classical ECG changes which are right bundle
branch block with ST elevation in leads V1–V3

Reference : Kumar and Clark 8th edition

42. E

Hereditary hemorrhagic telengienctasia (Osler-Weber-Rendu syndrome) is a autosomal dominant

condition which causes telengiectasia on the skin and mucus membranes. It also causes cerebral,
pulmonary and hepatic arterio-venous malformations. The given clinical scenario matches this
condition

PCKD doesn’t cause bleeding manifestations. But it has an autosomal dominant inheritance and causes
cerebral arterio-venous malformations

Chronic drug abuse leading to gastric erosion or CKD will not explain the father’s death due to a stroke

Drug induced aplastic anemia will involve all 3 cell lines. It also will not explain the father’s death

Ref: Oxford handbook of clinical medicine 9th edition

43. B

Features of polymyalgia rheumatica are Age >50yrs; subacute onset (<2 weeks) of bilateral aching,
tenderness and morning stiffness in shoulders and proximal limb muscles ± mild polyarthritis,

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tenosynovitis, and carpal tunnel syndrome (10%). Weakness is not a feature. There may be associated
fatigue, fever, weight loss, anorexia and depression.

To diagnose Infective endocarditis the duke’s criteria should be fulfilled.

Rheumatoid arthritis and SLE usually doesn’t usually have an axial involvement. (But RA can have
Atlantio-axial subluxation)

Ref: Oxford handbook of clinical medicine 9th edition

44. A (not sure)

Hump nosed viper causes nephrotoxicity, bleeding manifestations and local effects. Indian polyspecific
Anti venom cannot be given for hump nosed viper.

45. (Not sure)

47) key words are;

# 40 # male # hx of back pain # painful KJ
# stiffness >2hrs

Ankylosing Psoriatic Reiters Rheumatoid

spondylitis arthritis syndrome arthritis

Age early 30s 30-50 15-35 30-50

F:M 1:5 equally affected urogenital 1 : 2 3:1

enteral 1 : 3

joint Mainly Sacroiliac J Mono/Oligo/Poly Acute B/L symmetrical

involvement & Lumbar spine. arthritis asymmetrical polyarthritis
asymmetrical AS LL arthritis PIPJ

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 peripheral large J DIPJ usually after Cervical spine
involvement. Arthritis mutilans infection (
- telescopic dysentery/NSU/N
fingers SC)
sacroilitis

other pain worse in the Nail dystrophy Conjunctivitis morning stiffness

features morning relieved by often with DIPJ Circulate balanitis last >1hr
exercise. involvement. Urethritis joint deformities (
restricted neck Planter fasciitis z thumb ,
movements. Achilles tendinitis boutonniere ,ulnar
uveitis Keratoderma deviated MCPJ ,
costochondritis balanorrhagica swan neck
deformity)
CTS
Nodules
Anaemia

Ix elevated ESR & X- X-Ray - pencil in FBC - NCNC

ray spine - cup appearance anaemia
“bamboo spine” Elevated ESR &
syndesmophytes CRP
,calcification of X-Ray -
intervertebral J & Serology -
fusion of facet joints antiCCP ANA

Mx Exercises NSAIDs Antibiotics DMARDs

NSAIDs Sulfasalazine NSAIDs NSAIDs
Sulfasalazine MTX Sulfasanlazine antiTNF-alpha
MTX anti TNF-alpha MTX rituximab
antiTNF-alpha antiTNF-alpha

Most likely answer is A.

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48) key words are;
# 24 # female # bank officer- sedentary
# weight gain # lethargy # oligomenorrhoea
# high BP 170/100 # K+ low (<3.5) # Na+ slightly high (135 -145)
# TSH normal # Hb normal
Conn syndrome
● excess aldosterone production from adrenal cortex.
● <35 years
● hypokalemia
● adenomas are common in females
● weakness and sweat attacks
● Ix - raised ARR , raised plasma aldosterone , suppressed renin activity
, urinary potassium loss
# oligo menorrhea and weight gain can not be explained

Cushing syndrome

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 ● hypokalemia due to mineralocorticoid activity

Hypothyroidism
● hyponatremia due to increased ADH levels.
● high TSH confirms the disease but if TSH is normal or low then only low free T4 level confirms
the disease
# evidence to confirm hypothyroidism is lacking

Metabolic syndrome
# Electrolyte changes can not be explained.

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Obstructive sleep apnea
# oligo menorrhea and electrolyte changes can not be explained.

so Cushing syndrome is more likely.

49)
50) key words are,
# 45 # male # low grade fever × 5 days # headache
# myalgia # dry cough for few days # mild icterus
# bilateral crepitation # CXR - bilateral diffuse opacities in lower lobes

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 strep. strep. legionella myco. stap.
pneumoniae epidermidis pneumophila pneumoniae aureus

opportunistic atypical atypical

pathogen in pneumonia pneumonia
patients with
indwelling
devices.

clinical Acute onset Slow onset Slow onset Acute onset

features High fever Low grade Low grade High fever
Rust colour fever fever Rust colour
cough Dry cough Dry cough cough
Pleurisy More extra More extra Pleurisy

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 pulmonary pulmonary
symptoms symptoms

CXR consolidation lobal and one lobe, can multilobar

with air multilobar be bilateral consolidationc
bronchogram, shadowing. and extensive avitation
effusion and occasional lung pneumatocoel
collapse due to small involvment. e
retention of effusions.
secretions.

so the clinical picture is compatible with Mycoplasma pneumoniae infection. because it explains mild
icterus which is due to hemolysis.

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