IMAGE BASED QUESTIONS ( AUGUST 2024 ).pdf

This presentation contains 10 image based questions.

All are based on Harrison's Principles of Internal Medicine ( 21st edition )

There is a short description about the relevant topic with each question.

This was discussed with Internal Medicine PGs in Kerala.

1. IMAGE BASED QUESTIONS
AUGUST 2024

2. Instructions
●There are 10 image based questions in this set.


●The figure number / table number in the Harrison’s
Principles of Internal Medicine 21st edition is
mentioned with each image.

3. FIG 46-2

4. Q1. X & Y ?
Tonic contraction of the X muscle, which forms a sling around the
rectoanal junction, is important to maintain continence; during
defecation, sacral parasympathetic nerves relax this muscle,
facilitating the straightening of the rectoanal angle.
Distention of the rectum results in transient relaxation of the internal
anal sphincter via intrinsic and reflex sympathetic innervation. As
sigmoid and rectal contractions, as well as straining (Valsalva
maneuver), which increases intra abdominal pressure, increase the
pressure within the rectum, the rectosigmoid angle opens by >15°.
Voluntary relaxation of the external anal sphincter (striated muscle
innervated by the Y ) in response to the sensation produced by
distention permits the evacuation of feces.

5. ANSWERS
X - Puborectalis
The puborectalis is a muscle of the pelvic floor. It is part of the levator ani
muscle group, and the most important for maintaining faecal continence.

Y - Pudendal Nerve
●The pudendal nerve is a major somatic nerve of the sacral plexus.
●Nerve roots : S2-S4
●Sensory – innervates the external genitalia of both sexes and the skin
around the anus, anal canal and perineum
●Motor – innervates various pelvic muscles, the external urethral
sphincter and the external anal sphincter.

6. FIG 65-3

7. Q2. X & Y ?
Protein C is a plasma glycoprotein that becomes an anticoagulant when it is
activated by thrombin. The thrombin-induced activation of protein C occurs
physiologically on X , a transmembrane proteoglycan-binding site for thrombin
on endothelial cell surfaces. The binding of protein C to its receptor on
endothelial cells places it in proximity to the thrombin-X complex, thereby
enhancing its activation efficiency.
Activated protein C acts as an anticoagulant by cleaving and inactivating
activated factors V and VIII. This reaction is accelerated by a cofactor, Y ,
which, like protein C, is a glycoprotein that undergoes vitamin K–dependent
post translational modification.
Quantitative or qualitative deficiencies of protein C or Y , or resistance to the
action of activated protein C by a specific variant at its target cleavage site in
factor Va (factor V Leiden), lead to hypercoagulable states.

8. ANSWERS
X - Thrombomodulin

Y - Protein S

9. FIG 140 - 6

10. Q3.
1.Identify the marked dural venous sinuses (brown , blue , green , red )

2.Mention the predisposing conditions for dural venous sinus
thrombosis.

3.Mention the clinical features of cavernous sinus thrombosis.

4.What is Gradenigo’s syndrome ?

11. ANSWERS
1.
●Brown - Transverse sinus
●Blue - Straight sinus
●Green - sigmoid sinus
●Red - Cavernous sinus
2.
●Bacterial meningitis
●Subdural empyema /
Epidural abscess
●Dehydration from vomiting
●Hypercoagulable states
●Antiphospholipid syndrome

12. 3. The symptoms of septic cavernous sinus thrombosis are fever, headache,
frontal and retro orbital pain, and diplopia. The classic signs are ptosis,
proptosis, chemosis, and extraocular dysmotility due to deficits of cranial
nerves III, IV, and VI; hyperesthesia of the ophthalmic and maxillary divisions
of the fifth cranial nerve and a decreased corneal reflex may be detected.
There may be evidence of dilated, tortuous retinal veins and papilledema.

4. Gradenigo Syndrome (GS) is classically described as a clinical triad of otitis
media, facial pain and abducens palsy that is most commonly developed
from infection in the petrous temporal bone (i.e., petrous apicitis)

13. The cerebral veins and venous sinuses have no valves; therefore, blood
within them can flow in either direction.
The superior sagittal sinus is the largest of the venous sinuses . It
receives blood from the frontal, parietal, and occipital superior cerebral
veins and the diploic veins, which communicate with the meningeal veins.
The diploic veins, which drain into the superior sagittal sinus, provide a
route for the spread of infection from the meninges, especially in cases
where there is purulent exudate near areas of the superior sagittal sinus.

14. The superior sagittal sinus drains into the transverse sinuses .
The transverse sinuses also receive venous drainage from small veins
from both the middle ear and mastoid cells.
The transverse sinus becomes the sigmoid sinus before draining into
the internal jugular vein.
Septic transverse/sigmoid sinus thrombosis can be a
complication of acute and chronic otitis media or mastoiditis.
Infection spreads from the mastoid air cells to the transverse sinus via
the emissary veins or by direct invasion.

15. Emissary veins are valveless venous structures that connect
the extracranial vessels of the scalp to the intracranial dural
venous sinuses and diploic veins. They are a major route for
infectious agents to reach the brain's cerebral veins and venous
sinuses, and they also provide an alternative route for draining
blood from the brain.
Diploic veins are a network of valveless veins that run through the
diploe, the spongy layer of bone in the skull's cranial vault. They connect
the intracranial and extracranial venous systems, and provide alternative
routes for blood flow if there's a venous obstruction.

17. The cavernous sinuses are inferior to the superior sagittal sinus at the base of
the skull.
The cavernous sinuses receive blood from the facial veins via the superior and
inferior ophthalmic veins.
Bacteria in the facial veins enter the cavernous sinus via these veins. Bacteria
in the sphenoid and ethmoid sinuses can spread to the cavernous sinuses via
the small emissary veins.
The sphenoid and ethmoid sinuses are the most common sites of
primary infection resulting in septic cavernous sinus thrombosis.

18. The diagnosis of septic venous sinus thrombosis is suggested by an
absent flow void within the affected venous sinus on MRI and
confirmed by magnetic resonance venography, CT angiogram, or the
venous phase of cerebral angiography

19. FIG 253 - 1

20. Q4.
The ECGs ( Panel A & Panel B ) are recorded from two patients with family
history of sudden death.

1.What are the abnormalities in panel A ? What is the likely diagnosis ?

2.What are the abnormalities in panel B ? What is the likely diagnosis ?

3.Describe the genetic basis of these two conditions.

21. ANSWERS
1.T wave inversions in leads V1 - V3. Epsilon wave in V1 ; Arrhythmogenic right
ventricular cardiomyopathy ( ARVC )

2. ST elevation in V1 and V2 , suggestive of Brugada syndrome.

3.
ARVC - Due to mutations in genes encoding for cardiac desmosomal proteins
Brugada Syndrome - Mutations involving cardiac sodium channels are
identified in ~25% of cases.

22. ARRHYTHMOGENIC RIGHT VENTRICULAR
CARDIOMYOPATHY ( ARVC )
A rare genetic disorder most commonly due to mutations in genes
encoding for cardiac desmosomal proteins; however, it is increasingly
appreciated that other cardiomyopathic processes may produce a similar
phenotype.
Approximately 50% of patients have a familial transmission with
autosomal dominant inheritance.
Patients are typically diagnosed between the second and fifth decades
with palpitations, syncope, or cardiac arrest owing to sustained
monomorphic VT, although polymorphic VT can also occur.

23. Fibrosis and fibrofatty
replacement most
commonly involve the
right ventricular
myocardium and
provide the substrate
for reentrant VT that
usually has a left bundle
branch block–like
configuration in ECG
lead V1 , consistent with
the right ventricular
origin, and can
resemble idiopathic VT.
Gross photograph, showing dilation of the right ventricle and
near-transmural replacement of the right ventricular free-wall
by fat and fibrosis. The left ventricle has a virtually normal
configuration.

25. LV involvement can occur and can occasionally precede manifest right
ventricular disease. Clinical heart failure is rare except in late stages, and
survival to advanced age can be anticipated provided that VT can be
controlled.
An ICD is recommended.
When VT is exercise induced, it may respond to β-adrenergic blockers and
limiting exercise. Sotalol, flecainide, and amiodarone have been used to
reduce ventricular arrhythmias. Catheter ablation prevents or reduces VT
episodes in 70% of patients, but epicardial mapping and ablation are
often required.

26. BRUGADA SYNDROME
●Coved ST segment elevation >2mm in >1 of V1-V3 followed by
a negative T wave.
●This is the only ECG abnormality that is potentially diagnostic.
●It is often referred to as Brugada sign.

This ECG abnormality must be associated with one of the following
clinical criteria to make the diagnosis:
●Documented ventricular fibrillation (VF) or polymorphic
ventricular tachycardia (VT).
●Family history of sudden cardiac death at <45 years old .
●Coved-type ECGs in family members.
●Inducibility of VT with programmed electrical stimulation
●Syncope.
●Nocturnal agonal respiration.

Type 1

27. Brugada Type 2 has >2mm of saddleback shaped ST elevation.

Brugada type 3: can be the morphology of either type 1 or type 2, but
with <2mm of ST segment elevation.

Brugada syndrome is named after Spanish cardiologists Pedro and Josep
Brugada, who reported the condition as a distinct clinical syndrome in
1992.

28. Distinction from patients with similar ST elevation owing to LV hypertrophy,
pericarditis, myocardial ischemia or MI hyperkalemia, hypothermia, right
bundle branch block, and arrhythmogenic right ventricular cardiomyopathy is
often difficult. Furthermore, the characteristic ST-segment elevation can wax
and wane over time and may become pronounced during acute illness and
fever.
Administration of the sodium channel–blocking drugs flecainide, ajmaline, or
procainamide can augment or unmask ST elevation in affected individuals.

30. An ICD is indicated for individuals who have had unexplained
syncope or been resuscitated from cardiac arrest.
Quinidine and catheter ablation of abnormal regions in the epicardial
right ventricular free wall have been used successfully to suppress
frequent episodes of VT.

31. 308 - 2

32. Q5.
1.Mention a few etiologies of acute allergic interstitial nephritis

2. Mention a few infections causing acute interstitial nephritis

3. Mention the clinical features of acute interstitial nephritis

33. ANSWERS
1.Antibiotics ( Cephalosporins ,
Rifampicin , Penicillins , Sulfa
drugs , Quinolones ) ,
Allopurinol , Proton pump
inhibitors

2.TB , Leptospirosis ,
Mycoplasma , Legionella ,
Lyme disease

34. 3. Acute allergic or immune interstitial nephritis (AIN)
●Usually occurs 1 day to 2 weeks following exposure to an offending drug and
●May be associated with a rapid and potentially reversible loss of kidney
function, which may occur in the setting of a change in dose or the restarting of
a previously used medication.
●Associated glomerular proteinuria sometimes occurs with the use of
nonsteroidal anti-inflammatory drugs (NSAIDs) or ampicillin.
●Clinically, there may be fever, rash, and eosinophilia; the last is typical for
certain penicillins, fluoroquinolones, and some biologic cancer drugs that act as
checkpoint inhibitors (CPIs) but is atypical for NSAIDs.
●The urinalysis usually shows pyuria and at times eosinophiluria, but the most
characteristic cell types are activated T lymphocytes and plasma cells, along with
some white blood cell casts.
●The patient may experience symptoms of polyuria and tender kidneys, and
signs of tubular dysfunction including nephrogenic diabetes insipidus, hypo-
or hyperkalemia and hyperchloremic metabolic acidosis.

37. FIG 328-2

38. Q6.
1.What is a true intestinal diverticulum ?

2.What are the risk factors for bleeding from a diverticulum ?

3.What are the symptoms & signs of diverticulitis ?

4.What is this ( the image in the previous slide ) classification system of
diverticulitis known as ?

39. ANSWERS
1.A true diverticulum is a saclike herniation of the entire bowel
wall

2. Patients at increased risk for bleeding tend to be hypertensive,
have atherosclerosis, and regularly use antithrombotic therapy
and nonsteroidal anti-inflammatory agents. Additional risk
factors include obesity and a history of diabetes mellitus.

40. 3. Diverticulitis is inflammation of a diverticulum.
●Acute uncomplicated diverticulitis (also known as symptomatic
uncomplicated diverticular disease [SUDD]) characteristically
presents with fever, anorexia, left lower quadrant abdominal pain,
and obstipation.
●In <25% of cases, patients may present with generalized peritonitis
indicating the presence of a diverticular perforation.
●If a pericolonic abscess has formed, the patient may have abdominal
distention and signs of localized peritonitis.
4. Perforated diverticular disease is staged using the Hinchey
classification system

41. Diverticula commonly affect
the left and sigmoid colon; the
rectum is always spared.
However, in Asian populations,
70% of diverticula are seen in
the right colon and cecum as
well.

42. A pseudo diverticulum involves only a protrusion of the mucosa
and submucosa through the muscularis propria of the colon.
The type of diverticulum most commonly affecting the colon is the
pseudodiverticulum.

43. Hemorrhage from a colonic diverticulum is the most common
cause of hematochezia in patients >60 years, yet only 20% of
patients with diverticulosis will have gastrointestinal bleeding.
Most bleeds are self-limited and stop spontaneously with bowel rest.
The lifetime risk of rebleeding is 25%.

45. FIG 359-2

46. Q7.
Shown is the transthoracic echocardiographic image from a 5 year old boy with
chronic rheumatic heart disease.
1.What is the appearance of the anterior leaflet of the mitral valve ( in the image
shown in the previous slide ) known as ?

2.What are the investigations that should be always be requested in a patient
with suspected acute rheumatic fever ?

3.What is the recommended duration of secondary prophylaxis in a rheumatic
fever patient with persistent valvular disease ?

47. ANSWERS
1.Hockey stick or elbow deformity ( leaflet thickening, restriction of the
anterior mitral valve leaflet tip and doming of the body of the leaflet
toward the interventricular septum )

2. Always request:
●Electrocardiogram (ECG)
●Echocardiogram
●Complete blood count (CBC)
●C-reactive protein (CRP)
●Streptococcal serology (antistreptolysin and anti-DNase B)

48. 3. For 10 years after
the last attack, or 40
years of age
(whichever is longer);
sometimes lifelong
prophylaxis

49. FIG 381-4

50. Q8.
Shown is a simplified approach to the differential diagnoses
of diabetes insipidus.
1.Identify the red , violet and yellow boxes.

2.What is the significance of pituitary bright spot ?

3.Briefly outline the treatment of central diabetes insipidus.

51. ANSWERS
1.Red - Basal plasma
AVP
Violet - Primary
polydipsia
Yellow - Pituitary
Diabetes Insipidus

52. Diabetes insipidus (DI) is a syndrome characterized by the excretion of
abnormally large volumes of dilute urine.

The 24-h urine volume exceeds 40 mL/ kg body weight, and the 24-h urine
osmolarity is <280 mosm/L.

The polyuria produces symptoms of urinary frequency, enuresis, and/ or
nocturia. It also results in a slight rise in plasma osmolarity/sodium that
stimulates thirst and a commensurate increase in fluid intake (polydipsia).
Hence, clinical symptoms and signs of dehydration are uncommon unless
thirst and/or water intake are also impaired.
The most common form of DI is due to a primary deficiency of AVP secretion.
It is referred to variously as neurohypophyseal, neurogenic, pituitary, cranial,
or central DI. It can be caused by a variety of congenital, acquired, or genetic
disorders but is often idiopathic

53. 2. Posterior pituitary bright spot (PPBS) refers to an area of T1
hyperintensity in the posterior pituitary in MR imaging of the brain. It is
found in 80–90% of healthy children and adults.
The absence of posterior pituitary bright spot should prompt the
consideration of the following (noting it may be absent in normal patients):
●ectopic posterior pituitary
●central diabetes insipidus
●other diseases that disrupt the infundibuloneurohypophyseal system,
e.g. tumors, infection, inflammation
●empty sella

54. 3.
The signs and symptoms of uncomplicated pituitary DI can be
eliminated by treatment with desmopressin (DDAVP), a synthetic
analogue of AVP.
DDAVP acts selectively at V2 in a dose-dependent manner. It is also
more resistant to degradation than is AVP and has a three- to
fourfold longer duration of action.
DDAVP can be given by IV or SC injection, nasal inhalation, or orally
by means of a tablet or melt.

55. The doses required to control pituitary DI vary depending on the
patient and the route of administration.
However, among adults, they usually range from 1–2 μg qd or bid
by injection, 10–20 μg bid or tid by nasal spray, or 100–400 μg bid
or tid orally.
The onset of antidiuresis is rapid, ranging from as little as 15 min
after injection to 60 min after oral administration.

56. When given in a dose that normalizes 24-h urinary osmolarity
(400–800 mosmol/L) and volume (15–30 mL/kg body weight),
DDAVP produces a slight increase in total body water and a
(1–2%) decrease in plasma osmolarity/sodium that rapidly
eliminates thirst and polydipsia .
Consequently, water balance is maintained within the normal
range.

57. Hyponatremia rarely develops unless urine volume is reduced to
<10 mL/kg per day or fluid intake is excessive due to an associated
abnormality in thirst or cognition.
Fortunately, thirst abnormalities are rare, and if the patient learns to
drink only when truly thirsty, DDAVP can be given safely in doses
sufficient to normalize urine output without the need for allowing
intermittent escape to prevent water intoxication.

58. Q9. Identify the hidden boxes.

60. The choice of therapy in hypercalcemia depends on
●the underlying disease,
●the severity of the hypercalcemia,
●the serum inorganic phosphate level, and
●the renal, hepatic, and bone marrow function.


Hypercalcemia develops because of excessive skeletal calcium release,
increased intestinal calcium absorption, or inadequate renal calcium
excretion. Understanding the particular pathogenesis helps guide therapy.

61. Mild hypercalcemia ≤3 mmol/L [12 mg/dL]) can usually be managed by hydration.
Severe hypercalcemia (≥3.7 mmol/L [15 mg/dL]) requires rapid correction. IV
pamidronate or zoledronate or subcutaneous denosumab should be administered.
In addition, for the first 24–48 h, aggressive sodium-calcium diuresis with IV saline
should be given and, following rehydration, large doses of furosemide or ethacrynic
acid, but only if appropriate monitoring is available and cardiac and renal function
are adequate.
Intermediate degrees of hypercalcemia between 3 and 3.7 mmol/L (12 and 15
mg/dL) should be approached with vigorous hydration and then the most
appropriate selection for the patient of the combinations used with severe
hypercalcemia.

62. FIG 435 -1

63. Q10.
1.Identify the arrow marked structures.

2.Mention a few conditions where this is seen.

3.Mention a few conditions where deep brain
stimulation is useful.

64. ANSWERS
1.Lewy body
2.Parkinson’s disease , Dementia with Lewy bodies
3.Deep brain stimulation (DBS) is used for the treatment of
●Essential tremors,
●Epilepsy
●Dystonia,
●Parkinson disease, and
●Treatment-refractory obsessive-compulsive disease (OCD)

65. Lewy bodies are intraneuronal cytoplasmic inclusions that stain
with periodic acid–Schiff (PAS) and ubiquitin but are now identified
with antibodies to the presynaptic protein α-synuclein.
Lewy bodies are composed of straight neurofilaments 7–20 nm long
with surrounding amorphous material and contain epitopes
recognized by antibodies against phosphorylated and
nonphosphorylated neurofilament proteins, ubiquitin, and
α-synuclein.
The German neurologist named Friederich Lewy was the first
physician-scientist to describe the abnormal protein deposits in 1912 in
people with paralysis agitans.

66. Synucleinopathies (also called α-Synucleinopathies) are
neurodegenerative diseases characterised by the abnormal
accumulation of aggregates of alpha-synuclein protein in
neurons, nerve fibres or glial cells.


There are three main types of synucleinopathy:

●Parkinson's disease (PD),
●Dementia with Lewy bodies (DLB), and
●Multiple system atrophy (MSA).

67. DEEP BRAIN STIMULATION
The deep brain stimulation (DBS) apparatus consists of electrodes
implanted adjacent to specific deep brain structures, which are then
connected to a pacemaker-like machine (pulse generator) that is
implanted on the chest wall, via a subcutaneous wire. Stimulation
parameters are then relayed by a computer to the pulse generator,
appropriating proper amplitudes, frequencies, and pulse width.
Common structures targeted by DBS include the subthalamic nucleus
(STN), globus pallidus interna (GPi), and the ventral intermediate nucleus
of the thalamus (VIM).