Internal Medicine
1 questionsWhich disease does not recur in the kidney after a renal transplant?
NEET-PG 2015 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 771: Which disease does not recur in the kidney after a renal transplant?
- A. Alport syndrome (Correct Answer)
- B. Amyloidosis
- C. Goodpasture's syndrome
- D. Diabetic nephropathy (due to uncontrolled diabetes)
Explanation: **Alport syndrome** * **Alport syndrome** is a genetic disorder affecting type IV collagen, primarily in the kidney; recurrence is not observed in a renal allograft because the transplanted kidney provides new, healthy type IV collagen [2]. * The disease is due to a genetic defect in the recipient's collagen genes, so the transplanted kidney, which is genetically distinct, is not susceptible to the same primary disease process [2]. *Amyloidosis* * **Amyloidosis** can recur in the transplanted kidney, as it is a systemic disease where abnormal proteins continue to deposit in various organs, including the new kidney. * The underlying cause of amyloid production is typically not cured by a kidney transplant, making the new organ vulnerable to recurrence. *Goodpasture's syndrome* * **Goodpasture's syndrome** is an autoimmune disease where antibodies target type IV collagen in the glomerular basement membrane; these autoantibodies can attack the new kidney if they are still present at the time of transplant or re-emerge [1]. * Recurrence is a significant concern, although it can often be prevented by ensuring the patient is antibody-negative before transplantation and through immunosuppression [1]. *Diabetic nephropathy (due to uncontrolled diabetes)* * **Diabetic nephropathy** almost invariably recurs in the transplanted kidney if the recipient's diabetes remains uncontrolled after transplantation. * The metabolic environment, characterized by hyperglycemia, directly contributes to the damage of the new kidney, leading to the development of diabetic nephropathy over time.
Ophthalmology
9 questionsWhat is the cause of glaucoma in retinoblastoma?
What is the primary function of glaucoma drainage devices?
A 44-year-old woman presents with sudden painless loss of vision with a history of previous similar episodes. Fundoscopy shows no glow. What could be the possible diagnosis?
All of the following are true for retinopathy of prematurity except which of the following?
What is the primary predisposing factor for retinopathy of prematurity?
Which of the following statements is false regarding Eale's disease?
Purtscher's retinopathy is associated with -
What is the typical appearance of a subhyaloid hemorrhage in the eye?
Most common age related change in vitreous?
NEET-PG 2015 - Ophthalmology NEET-PG Practice Questions and MCQs
Question 771: What is the cause of glaucoma in retinoblastoma?
- A. Neovascularisation (Correct Answer)
- B. Mass effect of the tumour
- C. Blockage of trabecular network
- D. Lysis of the lens
Explanation: ***Neovascularisation*** - Retinoblastoma leads to **neovascularization of the iris (NVI)** and **angle structures** due to tumor necrosis, ischemia, and release of **angiogenic factors (VEGF)**. - The **neovascular membrane** grows over and obstructs the **trabecular meshwork** and anterior chamber angle, causing **secondary neovascular glaucoma**. - This is the **most characteristic and common mechanism** of glaucoma in advanced retinoblastoma. - Neovascular glaucoma in retinoblastoma is typically **refractory to medical treatment** and indicates poor prognosis. *Blockage of trabecular network* - While tumor cells can directly seed into the anterior chamber and block the trabecular meshwork, this mechanism is **less common** than neovascularization. - This option is also **less specific** as it doesn't identify the underlying pathophysiological process (neovascularization) that is characteristic of retinoblastoma-associated glaucoma. - Direct trabecular blockage by tumor cells typically occurs in advanced disease and often coexists with neovascularization. *Mass effect of the tumour* - The tumor mass itself rarely causes glaucoma through direct mechanical compression of outflow pathways. - Retinoblastoma causes glaucoma primarily through **secondary mechanisms** such as inflammation, neovascularization, or cellular seeding, not simple bulk effect. - Massive tumors may cause angle closure, but this is uncommon compared to neovascular mechanisms. *Lysis of the lens* - **Phacolytic glaucoma** from lens protein leakage is rare in retinoblastoma. - While lens damage can occur with advanced tumors, it is **not a typical or characteristic cause** of glaucoma in retinoblastoma. - The primary mechanisms involve the **tumor-angle-trabecular meshwork axis**, not lens pathology.
Question 772: What is the primary function of glaucoma drainage devices?
- A. Drain aqueous humour to the posterior segment
- B. Drain aqueous humour to an external device (Correct Answer)
- C. Open the trabeculae mechanically
- D. Reduce the aqueous secretion by compressing the ciliary epithelium
Explanation: **Drain aqueous humour to an external device** - Glaucoma drainage devices create an artificial outflow pathway, channeling excess **aqueous humour** from the anterior chamber to an external reservoir (usually under the conjunctiva) to lower intraocular pressure. - This bypasses the compromised natural drainage system, preventing further damage to the **optic nerve**. *Drain aqueous humour to the posterior segment* - Glaucoma drainage devices are designed to drain aqueous humour from the **anterior segment** (specifically the anterior chamber) of the eye, not the posterior segment. - The posterior segment primarily contains the **vitreous humour**, and drainage to this area is not the intended mechanism for IOP reduction. *Open the trabeculae mechanically* - Glaucoma drainage devices do not mechanically open the **trabecular meshwork**; this is the mechanism of action for procedures like goniotomy or trabeculoplasty. - These devices create an entirely new drainage pathway, bypassing the dysfunctional trabecular meshwork. *Reduce the aqueous secretion by compressing the ciliary epithelium* - Reducing aqueous humour secretion is the mechanism of action for medications like **beta-blockers** or **carbonic anhydrase inhibitors**, which act on the **ciliary epithelium**. - Glaucoma drainage devices focus on increasing outflow, not on reducing the production of aqueous humour.
Question 773: A 44-year-old woman presents with sudden painless loss of vision with a history of previous similar episodes. Fundoscopy shows no glow. What could be the possible diagnosis?
- A. Vitreous Hemorrhage (Correct Answer)
- B. Rhegmatogenous Retinal Detachment
- C. Acute Angle-Closure Glaucoma
- D. Fungal Keratitis
Explanation: ***Vitreous Hemorrhage*** - **Painless vision loss** is a hallmark symptom, and **previous similar episodes** suggest a recurrent condition, characteristic of vitreous hemorrhage from fragile vessels. - The **"no glow"** on fundoscopy indicates that light from the ophthalmoscope is unable to reflect off the retina due to something obstructing the clear media, such as blood in the vitreous cavity. *Rhegmatogenous Retinal Detachment* - While it causes **painless vision loss**, patients often report **floaters** or **flashes of light** preceding the detachment, which are not mentioned here. - Fundoscopy in rhegmatogenous retinal detachment would typically show a **grayish, elevated retina**, often with folds, not a complete loss of red reflex or ''no glow.'' *Acute Angle-Closure Glaucoma* - Characterized by **sudden, severe eye pain**, blurred vision, and often a **red eye** with a fixed, mid-dilated pupil. - Fundoscopy would typically reveal a **cupped optic disc** in advanced stages, but the primary finding is elevated intraocular pressure, with a clear vitreous, thus allowing an initial glow. *Fungal Keratitis* - This is an **infection of the cornea** that typically presents with pain, redness, photophobia, and a visible corneal ulcer or infiltrate. - Vision loss is gradual, and fundoscopy would still show a **normal red reflex** unless the corneal opacity is extremely dense, which is not implied by "no glow."
Question 774: All of the following are true for retinopathy of prematurity except which of the following?
- A. Due to hypoxia there occurs neovascularization followed by fibroproliferation
- B. Occurs in premature infants due to abnormal retinal blood vessel development.
- C. End result is bilateral blindness (Correct Answer)
- D. Blindness can be prevented by early diagnosis and ablation of avascular peripheral retina with cryotherapy or photocoagulation
Explanation: ***End result is bilateral blindness*** - While retinopathy of prematurity (ROP) can lead to severe vision loss or blindness, it is not always a bilateral end result, especially with early diagnosis and treatment. The severity can vary between eyes, and some cases resolve spontaneously. - Modern screening and intervention strategies, such as laser photocoagulation or anti-VEGF injections, are often successful in preventing complete blindness in one or both eyes. *Due to hypoxia there occurs neovascularization followed by fibroproliferation* - This statement accurately describes the pathogenesis of ROP. The initial phase involves delayed normal retinal vascularization, followed by a proliferative phase characterized by **neovascularization** in response to hypoxia in the avascular retina. - These new, abnormal vessels are fragile and prone to bleeding, and their associated **fibrovascular proliferation** can lead to retinal detachment. *Blindness can be prevented by early diagnosis and ablation of vascular premature retina with cryotherapy or photocoagulation* - This is a true statement. **Early diagnosis** through ophthalmologic screening of premature infants is crucial, and treatments like **laser photocoagulation** or **cryotherapy** are effective in ablating the avascular peripheral retina to halt the progression of abnormal vessel growth. - These interventions reduce the hypoxic drive that fuels neovascularization, thereby preventing severe retinal detachment and subsequent blindness. *Occurs in premature infants due to abnormal retinal blood vessel development.* - This statement is correct. ROP is a disease primarily affecting **premature infants** because their retinal blood vessels have not completed development by the time of birth. - Postnatal factors, including oxygen fluctuations and low birth weight, further disrupt this critical development, leading to **abnormal vascularization**.
Question 775: What is the primary predisposing factor for retinopathy of prematurity?
- A. Oxygen toxicity
- B. Carbohydrate excess
- C. Low birth weight
- D. Low gestational age (Correct Answer)
Explanation: ***Low gestational age*** - **Prematurity** is the most significant risk factor, as the **retinal vasculature** is still immature and susceptible to abnormal development. - The earlier the gestational age, the **higher the risk** of ROP developing and progressing to severe stages. *Low birth weight* - While strongly correlated with ROP, **low birth weight** is often a consequence of prematurity rather than the primary predisposing factor itself. - Many term infants can have low birth weight due to **intrauterine growth restriction** but do not typically develop ROP. *Oxygen toxicity* - **Supplemental oxygen** can exacerbate ROP by causing initial **vasoconstriction** and subsequent abnormal vessel proliferation. - However, it acts as a secondary trigger in an already vulnerable, premature retina, not the primary predisposing factor. *Carbohydrate excess* - **Carbohydrate excess** is not a recognized predisposing factor for retinopathy of prematurity. - This condition is primarily related to the **vascular development of the retina** in premature infants.
Question 776: Which of the following statements is false regarding Eale's disease?
- A. Optic neuritis (Correct Answer)
- B. AKT is given
- C. Vitreous Hemorrhage
- D. Retinal detachment may occur
Explanation: ***Correct Answer: Optic neuritis*** - This statement is **false** because **Eale's disease** is a **peripheral retinal vasculitis** (periphlebitis) that primarily affects the **peripheral retinal veins**. - The condition does **NOT involve the optic nerve**, and **optic neuritis is NOT a recognized feature or complication** of Eale's disease. - The disease process is confined to the retinal vasculature and does not extend anteriorly to involve the optic disc or nerve in typical cases. *AKT is given* - While the exact etiology of Eale's disease remains uncertain, there is a **historical and clinical association with tuberculosis**, particularly in TB-endemic regions like India. - In clinical practice, **anti-tubercular therapy (ATT/AKT) is often empirically administered** when TB cannot be ruled out or when there is suspicion of systemic TB. - Some studies suggest ATT may help reduce inflammation and prevent recurrence in selected cases. *Vitreous Hemorrhage* - This is a **hallmark complication** of Eale's disease, particularly in stage 3 (proliferative stage). - **Recurrent vitreous hemorrhage** occurs due to rupture of fragile neovascular vessels that form in response to retinal ischemia. - It is one of the most common presentations requiring intervention. *Retinal detachment may occur* - **Tractional retinal detachment** is a recognized complication resulting from contraction of **fibrovascular proliferative membranes**. - **Rhegmatogenous retinal detachment** can also occur if vitreoretinal traction causes retinal breaks. - Both types may require surgical intervention (vitrectomy).
Question 777: Purtscher's retinopathy is associated with -
- A. Head trauma (Correct Answer)
- B. Diabetes Mellitus
- C. Wilson's disease
- D. Rheumatoid arthritis
Explanation: ***Head trauma*** - **Purtscher's retinopathy** is a rare occlusive microvasculopathy characterized by sudden vision loss and specific retinal findings, classically associated with **head or chest trauma**. - The condition occurs due to **fat embolization** and **leukoembolization** with complement activation, leading to occlusion of retinal precapillary arterioles. - Classic findings include **cotton wool spots**, intraretinal hemorrhages, and **Purtscher flecken** (polygonal areas of retinal whitening between the optic disc and macula). - The term "Purtscher's retinopathy" specifically refers to trauma-induced cases, while "Purtscher-like retinopathy" describes similar findings from non-traumatic causes (acute pancreatitis, fat embolism syndrome, amniotic fluid embolism). *Diabetes Mellitus* - **Diabetic retinopathy** is associated with chronic hyperglycemia causing microvascular damage, characterized by microaneurysms, dot-blot hemorrhages, hard exudates, and venous beading. - It involves gradual progressive changes over years, not acute embolic occlusion from trauma. - Advanced stages include **proliferative diabetic retinopathy** with neovascularization and diabetic macular edema. *Wilson's disease* - **Wilson's disease** is an autosomal recessive disorder of copper metabolism affecting the liver, brain, and eyes. - Ocular manifestations include **Kayser-Fleischer rings** (copper deposition in Descemet's membrane) and sunflower cataracts. - It does not cause acute retinal vascular occlusion or the specific findings of Purtscher's retinopathy. *Rheumatoid arthritis* - **Rheumatoid arthritis** is a chronic autoimmune inflammatory disease primarily affecting joints. - Ocular manifestations include **keratoconjunctivitis sicca** (dry eyes), **episcleritis**, **scleritis**, and peripheral ulcerative keratitis. - It is not associated with Purtscher's retinopathy, which is specifically linked to traumatic or embolic events.
Question 778: What is the typical appearance of a subhyaloid hemorrhage in the eye?
- A. Boat shaped (Correct Answer)
- B. Crescent shaped
- C. Round
- D. Flame shaped
Explanation: ***Boat shaped*** - A subhyaloid hemorrhage is located beneath the **hyaloid membrane** (the posterior vitreous cortex), which is attached to the retina. - The collected blood often assumes a **dependent, gravity-influenced shape**, appearing flat on top and curved underneath, resembling a boat. *Crescent shaped* - This shape is not characteristic of a typical subhyaloid hemorrhage; it might be seen in other types of hemorrhages or detachment patterns. - **Crescentic shapes** are more commonly associated with certain types of **retinal detachments** or tears where fluid accumulation takes on a curved boundary. *Round* - While hemorrhages can be round, a subhyaloid hemorrhage typically spreads out due to gravity within the confined space, resulting in a more distinct shape. - A **perfectly round hemorrhage** is less common in the subhyaloid space as blood tends to layer out rather than remain as a sphere. *Flame shaped* - **Flame-shaped hemorrhages** are typically found in the **nerve fiber layer** due to the orientation of nerve fibers. - These hemorrhages are shallower and follow the linear arrangement of nerve fibers, unlike the larger, more globular subhyaloid bleeds.
Question 779: Most common age related change in vitreous?
- A. Anterior vitreous detachment
- B. Vitreous hemorrhage
- C. Vitritis
- D. Posterior vitreous detachment (PVD) (Correct Answer)
Explanation: ***Posterior vitreous detachment (PVD)*** - As we age, the **vitreous body** undergoes liquefaction and shrinkage, leading to its separation from the **retina**, most commonly posteriorly. - This is a very common and usually benign age-related phenomenon, often presenting with **floaters** and **flashes of light**. *Anterior vitreous detachment* - **Anterior vitreous detachment** is much less common than PVD and not typically considered the most frequent age-related change. - It often occurs secondary to **trauma** or specific surgical procedures rather than spontaneous aging alone. *Vitreous hemorrhage* - **Vitreous hemorrhage** is a pathological condition involving bleeding into the vitreous humor, often due to **diabetic retinopathy**, retinal tears, or trauma. - It is not a normal age-related change but a complication of underlying disease. *Vitritis* - **Vitritis** refers to inflammation of the vitreous humor, commonly associated with **uveitis** or infections. - It is an inflammatory disease process, not a physiological age-related degeneration of the vitreous.