Neurology, Urology & Cardiovascular System related Surgery PPT

PriyankaSwarnakar 8 views 87 slides May 14, 2025
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About This Presentation

Student friendly MCQ based presentation


Slide Content

NEUROSURGERY MCQ-BASED PREPARATIONS (AIAPGET) DR. SOUMYADIP PAL, B.H.M.S. , MD (HOM.)

HEAD INJURIES Skull Base Fractures Anterior Cranial Fossa Fracture Middle Cranial Fossa Fracture MC type of skull base fracture Caused by fracture of cribriform plate Clinical features: Subconjunctival hematoma CSF rhinorrhea Epistaxis, Anosmia Periorbital hematoma / Raccoon eyes Carotico-cavernous fistula Frontal lobe contusion Caused by fracture of petrous part of temporal bone Clinical features: CSF otorrhea Paradoxical rhinorrhea Hemotympanum Battle sign Ossicular disruption VII & VIII cranial nerve palsies Temporal lobe contusion Posterior Cranial Fossa Fracture Caused by fracture of occipital bone Clinical features: Visual disturbances VI cranial nerve injury Jugular foramen syndrome Paresis of IX, X, XI cranial nerves Basilar artery injury Occipital contusion

Skull base fractures

Brain abscess Intracerebral abscess may occur as a result of direct spread from air sinus infection , following surgery or from hematogenous spread. Etiology – Otitis media, mastoiditis; Paranasal sinusitis, dental infections; Hematogenous Location – Temporal lobe > Cerebellum; Clinical Features Presentation is with focal signs, seizures and raised ICP , as with other mass lesions, but the time course is often short Patients may be febrile or have a raised peripheral white cell count or inflammatory markers. Diagnosis – IOC for diagnosis: MRI CT scan: Ring-enhancing mass lesion (may be multiple in case of hematogenous spread)

Normal pressure hydrocephalus Characterized by the clinical triad of: Ataxic gait Dementia (usually mild to moderate, with an emphasis on executive impairment) Urinary urgency or incontinence This syndrome is a communicating hydrocephalus with a patent aqueduct of Sylvius. NPH maybe caused by obstruction to normal CSF flow over the cerebral convexities and delayed resorption into the venous system. The indolent nature of the process results in enlarged lateral ventricles with relatively little increase in CSF pressure. Diagnosis – MRI: Enlarged lateral ventricles with little or no cortical atrophy Lumbar puncture opening pressure falls in the high normal range CSF protein, glucose and cell counts are normal.

Brain tumours MC primary brain tumor – Meningioma (35%) > glial tumours (30%) MC malignant BT of childhood & Most radiosensitive BT – Medulloblastoma BT associated with calcification (COM) – Craniopharyngioma (most) > ODGG (90%) > Meningioma (20—25%) ASTROCYTOMA: Astrocytoma is MC posterior fossa tumor in children MC astrocytoma in children: Pilocytic astrocytoma MC astrocytoma in adults: Glioblastoma multiforme (GBM) OLIGODENDROGLIOMA: Characterized by classic histologic feature of "fried egg" cytoplasm, "chicken wire" vasculature , and microscopic calcifications.

Brain tumours CRANIOPHARYNGIOMA: Craniopharyngiomas are benign cystic lesions that occur most frequently in children . Derived from Rathke's pouch and arise near the pituitary stalk, commonly extending into the suprasellar cistern. Associated with hypopituitarism (90%), diabetes insipidus (10%) & growth retardation.

CARDIOTHORACIC SURGERY MCQ-BASED PREPARATIONS (AIAPGET) DR. SOUMYADIP PAL, B.H.M.S. , MD (HOM.)

ARTERIAL OCCLUSION Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

ARTERIAL OCCLUSION Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

arterial ulcers Arterial insufficiency ulcers ischemic ulcers are mostly located on the lateral surface of the ankle or the distal digits. Most common on distal ends of limbs. Etiology – Caused by lack of blood flow to the capillary beds of lower extremities. Most often endothelial dysfunction is causative factor in diabetic microangiopathy & macroangiopathy Characteristic Features – Punched-out appearance Pulses are not palpable Intensely painful Diagnosis – Arterial doppler & pulse volume recordings for baseline assessment of blood flow.

EMBOLIC OCCLUSION An embolus is detached thrombus from heart or a more proximal vessel. MC Source : Left atrium in atrial fibrillation >Mural thrombus following MI Clinical Features The leg is often affected, with pain, pallor, paresis, loss of pulsation & paranesthesia (or anesthesia). Movement becomes progressively more difficult and sensation is lost. Pulses are absent distally but the femoral pulse may be palpable. Diagnosis Made clinically in a patient who has no history of claudication and has a source of emboli, who suddenly develops severe pain or numbness of the limb, which becomes cold & mottled. Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

EMBOLIC OCCLUSION Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

BUERGER’S DISEASE / THROMBOANGITIS OBLITERANS Segmental inflammatory disease, affecting small & medium sized arteries in upper & lower extremities Definite relationship with smoking Histopathology Sharply segmental acute & chronic vasculitis of small & medium vessels with thrombosis of lumen which may undergo organization & recanalization. Thrombus contains micro abscesses. Clinical Features (RIM) Characterized by triad of intermittent claudication , Raynaud's phenomenon & migratory superficial vein thrombophlebitis. Typically seen in young (< 40 years), male smokers [Not seen in females & non-smokers]. Patient initially presents with foot, leg, arm or hand claudication progressing to rest pain and ulcerations on the toes, feet or fingers. TAO principally affects distal (small & medium) & hands .

Diagnosis Angiography of all four limbs (multiple limbs may be involved) Characteristic angiographic findings: Disease confinement to the distal circulation, usually infra-popliteal and distal to the brachial artery. Occlusions are segmental and show “Skip" lesions with extensive collateralization, the so-called “Corkscrew collaterals” BUERGER’S DISEASE / THROMBOANGITIS OBLITERANS Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

Arteriovenous fistula Communication between an artery & vein: congenital or acquired. MC type Of AVF: Congenital. MC cause Of acquired AVF: Penetrating trauma. Structural effects on veins: Veins are arterialized (become dilated, tortuous & thick walled) Physiological Effects of AVF Increased pulse pressure (Increased systolic & decreased diastolic) Increased venous return leading to increased HR & increased CO Left ventricular enlargement and later cardiac failure may occur Clinical Signs A pulsatile swelling Thrill on palpation Continuous bruit on auscultation Nicoladoni’s / Branham's sign: Pressure on artery proximal to fistula causes the swelling to diminish in size, a thrill or bruit to cease, the pulse rate to fall & the pulse pressure returns to normal. Diagnosis – Duplex scan and/or angiography confirm the diagnosis.

Raynaud's phenomenon & DISEASE Raynaud's phenomenon is characterized by episodic digital ischemia on exposure to cold or emotional stress . Manifested by the sequential development of digital blanching, cyanosis & rubor (redness) of fingers or toes Raynaud's phenomenon is divided into: Primary or idiopathic (Raynaud's disease) Secondary (associated with other diseases): Migraine/variants angina; Sclerodactyly Raynaud’s Disease: Majority (70-90%) of patients are young women < 40 years of age . Fingers are involved more commonly than toes. On examination, patient is entirely normal. Radial, ulnar and pedal pulses are normal.

Raynaud's phenomenon Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

Aortic dissection Aortic dissection is caused by a circumferential or, less frequently, transverse tear of the intima. MC site: Right lateral wall of the ascending aorta. Peak incidence: 6th & 7th decades Men are more commonly affected. Acute aortic dissection: Sudden onset of pain, very severe and tearing, associated with diaphoresis.

Aortic dissection Physical findings: Hypertension or hypotension, loss of pulses, aortic regurgitation, pulmonary edema„ and neurologic findings due to carotid artery obstruction (hemiplegia, hemianesthesia) or spinal cord ischemia (paraplegia). Signs of aortic regurgitation: Bounding pulses, a wide pulse pressure, a diastolic murmur often radiating along the right sternal border, and evidence of CHF. Pleural effusion (usually left-sided), typically serosanguineous is seen. Diagnosis CXR: widened superior mediastinum IOC for diagnosis in stable patients: CT angiography IOC for diagnosis in unstable patients: Transesophageal echocardiography Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

Aortic dissection Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

aneurysm Aneurysm: Permanent & irreversible localized dilatation of blood vessel with at least 50% increase in diameter. Ectasia: dilatation < 50% of normal diameter. MC vessel involved in aneurysm: Circle of Willis. MC location Of extra-cranial aneurysm: Aorta > Iliac > Popliteal > Femoral. MC site of extra-cranial arterial aneurysm is infrarenal aorta. MC site of peripheral aneurysm: Popliteal aneurysm. Degenerative aneurysms (caused by atherosclerosis) are most common – AAA Width of aneurysm is most important predicting factor of rupture. Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

Abdominal aortic aneurysm (AAA) MC site of aortic aneurysm is infrarenal aorta. AAA is diagnosed if diameter > 3 cm in males or >2.6 cm in females Risk Factors: Age, male gender, white race, smoking and family history Clinical Presentation Rupture is most common & most lethal complication. Most rupture occurs in left retroperitoneal space , others in abdominal cavity, IVC, iliac vein or duodenum (4th part- Most Common) Growth rate of AAAs vary with size, more rapid growth seen in aneurysms 5 cm or larger . Most Common Symptom: Chronic vague abdominal or back pain. Triad of aortic rupture: Sudden onset midabdominal or flank pain + Shock + Pulsatile abdominal mass .

Plain X-ray detects AAA in up to 70% cases by characteristic "eggshell" pattern of calcification Negative abdominal radiograph doesn't exclude the diagnosis. CT is IOC for diagnosis & planning repair in AAA MRI is IOC for diagnosis and with MR angiography planning repair in AAA with renal insufficiency. Abdominal aortic aneurysm – dx Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

Subclavian artery stenosis MC cause of subclavian artery stenosis: Atherosclerotic disease. Left subclavian artery stenosis is significantly more common than right. MC site of stenosis: First part of subclavian artery. Stenosis typically occurs just distal to origin of subclavian artery & lies proximal to origin of vertebral artery. Stenosis of first part of subclavian artery may give rise to Subclavian steal syndrome. Subclavian steal syndrome is characterized by reversed flow in vertebral artery to compensate for a proximal stenosis in the ipsilateral subclavian artery there by stealing blood from the 'brain' to feed the 'arm’. Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

Takayasu’s arteritis Rare, well-recognized chronic inflammatory arteritis affecting large vessels, predominantly the aorta & its main branches . Chronic inflammation leads to wall thickening, fibrosis, stenosis, & thrombus formation . Clinical Features Occurs predominantly in adolescent girls and young women, age of 10-40 years. Subclavian artery is MC involved vessel leading to loss or weakening of pulses (Pulseless Disease). Characteristic clinical features: Hypertension reflecting renal artery stenosis, retinopathy, cerebrovascular symptoms, angina and congestive heart failure, abdominal pain or GI bleeding or extremity claudication. Diagnosis IOC for diagnosis: CT angiography. Gold standard for diagnosis: Angiography.

Deep vein thrombosis Clinical Features – MC presentation of DVT: Pain & swelling, especially in the calf of one lower limb. Bilateral DVT is common, occurring in up to 30% May first present with signs of a pulmonary embolism , e.g. pleuritic chest pain, hemoptysis & shortness of breath. Physical signs: Mild pitting edema of the ankle, dilated surface veins, a stiff calf and tenderness over the course of the deep veins. Earliest sign of DVT: Calf tenderness. Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

Deep vein thrombosis

Deep vein thrombosis – dx Diagnosis – D-dimer measurement: If normal, no indication for further investigation but, if raised, a duplex ultrasound examination of the deep veins should be performed. Duplex ultrasound: Investigation of choice for diagnosis of DVT (Filling defects in flow and lack of compressibility indicate the presence of a thrombosis). Ascending venography: Shows thrombus as a filling defect, is now rarely required. Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

Varicose veins Varicose veins are dilated, tortuous elongated superficial veins ≥ 3 mm in diameter measured in upright position with demonstrable reflux. Most develop in the tributaries of the greater and lesser saphenous veins , which are usually dilated but rarely varicose themselves. Usual distribution of varicose veins is below the knee in branches of greater saphenous system. Varicosities in the thigh: Long saphenous incompetence Varicosities on the back of the leg: Short saphenous incompetence. Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

Varicose veins Pathophysiology – Defective connective tissue & smooth muscle in the vein wall leading to a secondary incompetence of the valves. Clinical Features – MC symptom: Dull aching pain in the veins at the end of the day, after prolonged standing Other symptoms: Ankle swelling, itching, bleeding, superficial thrombophlebitis, eczema, lipodermatosclerosis and ulceration. Diagnosis – Duplex ultrasound: Investigation of choice for diagnosis of varicose veins.

Varicose veins Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

Varicose veins Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

Venous ulcers Venous ulcer: Sloping edge, base contains granulation tissue covered by slough and exudate. Venous ulcer of the leg characteristically develops in the skin of the gaiter region, the area between muscles of the calf & ankle. Majority of ulcers develop on the medial side of the calf. Ulcers associated with lesser saphenous incompetence often develop on the lateral side of the leg. Almost all venous ulcers have surrounding lipodermatosclerosis (thickening, pigmentation, inflammation & induration of calf skin). Pigmentation comes from hemosiderin & melanin. Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

Venous ulcers – c/f & DX Presence of an ankle flare suggests venous hypertension. Inverted Champagne bottle leg is seen in varicose veins . DIAGNOSIS Duplex ultrasound: Assess the state of deep & superficial veins (IOC) Bipedal ascending phlebography: Detect obstruction & post-thrombotic changes missed by the duplex scan Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

lymphedema

Secondary lymphedema Secondary lymphedema is far more common than primary lymphedema. Secondary lymphedema develops as a result of lymphatic obstruction or disruption. Other causes of secondary lymphedema include radiation therapy, trauma, infection, and malignancy Globally, filariasis (caused by Wucheriria bancrofti, Brugia malayi, and Brugia timori ) is the most common cause of secondary lymphedema. Filariasis: MC cause of lymphedema worldwide. Dx – Lymphangiography Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

Stages of lymphedema

mediastinum MC anterior Mediastinal Masses: Thymoma MC middle MM: Cyst (Pericardial cyst is MC) MC posterior MM: Neurogenic tumors MC MM (overall): Neurogenic tumors MM seen in all three compartments of mediastinum: Lymphoma, bronchogenic cyst & mesenchymal tumors IOC for diagnosis of MM (except neurogenic tumors ): CT IOC for diagnosis of neurogenic tumors : MRI

Vascular anomalies PORT – WINE STAIN A vascular malformation Present at birth Grows along with the child Do not regress Face involvement in areas supplied by 5 th cranial nerve STRAWBERRY ANGIOMAS Type of capillary hemangioma Baby is normal at birth Appears at the age of 1—3 weeks Grows with the child up to I year of age and then cease to grow Emptying sign is demonstrable SALMON PATCH Also known as Macular stain or stork bite Present at birth Seen over forehead in the midline and over the occiput Disappears by the age 1 year

Vascular anomalies PORT – WINE STAIN STRAWBERRY ANGIOMAS SALMON PATCH

BERRY’S ANEURISM MC type of intra-cranial aneurysm. About 85% aneurysms occur in the anterior circulation, on the circle of willis. Predisposing factors: Smoking and hypertension. Wall of Berry aneurysm is made up of thickened hyalinized intima. Rupture of aneurysm usually occurs at the apex (dome) resulting in subarachnoid haemorrhage or intraparenchymal haemorrhage or both. Unruptured aneurysms are usually completely asymptomatic. Occurrence of Berry aneurysm in order of frequency Anterior communicating artery- Anterior Cerebral junction (29%) Posterior communicating artery-Internal carotid junction (28%) Middle cerebral bifurcation (18%) Intracranial carotid bifurcation (8%) Vertebrobasilar or basilar bifurcation (3%) Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

INCREASED RISK OF BERRY ANEURISM Coarctation of aorta Autosomal dominant Polycystic Kidney Marfan’s syndrome Ehlers-Danlos syndrome Fibromuscular dysplasia Mnemonic: CAM EF

Ischemic Hemorrhagic CAUSES OF CEREBROVASCULAR ACCIDENTS Embolic (75%) Thrombotic (25%) Parenchymal (10%) Subarachnoid (1-2%) Epidural (<1%) Subdural (<1%) INTRACEREBRAL (PARENCHYMAL) HEMORRHAGE SUBARACHNOID HEMORRHAGE MC type of intracranial hemorrhage. MC cause is hypertension, causing rupture of small perforating arteries or arterioles. MC site: Basal ganglia (Putamen). 2nd MC cause of intracranial hemorrhage. MC cause: Trauma > Spontaneous rupture of Berry aneurysm. MC site of Berry aneurysm is anterior circulation of “circle of willis”. Dr. SOUMYADIP PAL, B.H.M.S., MD (Hom.)

SUB-ARACHNOID HEMORRHAGE (SAH) MC cause: Trauma > Spontaneous rupture of Berry aneurysm. Clinical Features • Sudden transient loss of consciousness. • Excruciating severe headache: presenting complaint in 45% of cases (worst headache of patients life). • Neck stiffness and vomiting. • Sudden headache in the absence of focal neurological deficit is the hallmark of aneurysmal rupture. • Associated prodromal symptoms: Third cranial nerve palsy, Sixth nerve palsy, Aneurysm in cavernous sinus, Occipital and posterior cervical pain (Inferior cerebellar artery aneurysm), Pain in or behind the eye (MCA aneurysm). Diagnosis • Non contrast CT scan: Investigation of choice • CSF picture: Hallmark of aneurysmal rupture is blood in CSF (Xanthochromic spinal fluid). • Lumbar puncture should be performed if the CT scan fails to establish the diagnosis of SAH.

hematoma

SUBDURAL HEMATOMA EXTRADURAL HEMATOMA EDH is a neurosurgical emergency mostly associated with a skull fracture . More common in young male patients. Associated with tearing of a meningeal artery. Hematoma accumulates in the space between bone and dura . MC site: Temporal (pterion is thinnest part of skull and overlies middle meningeal artery) Not always arterial: disruption of a major dural venous sinus can result in an EDH. Classical presentation: Initial injury followed by a lucid interval (occurring in <1/3rd of cases). Early recognition and treatment is likely to result in full recovery & Delays in diagnosis and treatment can result in death from secondary brain injury. EDH on CT scan: Lentiform (lens shaped or biconvex) hyperdense lesion between the skull and brain. Treatment of EDH: Immediate surgical evacuation via a craniotomy. SDH accumulates in the space between dura and arachnoid . Disruption of a cortical vessel or brain laceration . Nearly always associated with a significant primary brain injury. Classification of SDH: Acute SDH: <3 days. Subacute SDH: 4-21 days. Chronic SDH: >21 days. Patients present with an impaired conscious level from the time of injury, but further deterioration can occur as the hematoma expands. CT appearance of SDH: Hyperdense (acute blood) concave appearance. Treatment of SDH : Evacuation via craniotomy. Small hematomas with little mass effect may be managed conservatively in neurosurgical centers. Mortality rate from SDH is much higher than for EDH and is as high as 40% in some series.

SURGICAL UROLOGY MCQ-BASED PREPARATIONS (AIAPGET) DR. SOUMYADIP PAL, B.H.M.S. , MD (HOM.)

Renal calculi – types Calcium oxalate stones Most Common type of kidney stone. Risk factors are hypercalciuria, hypercalcemia, hyperoxaluria. Have hard, small and jagged surface. Uric acid stones Most Common radiolucent urinary calculi, formed in acidic urine. Patients with uric acid stones may have hyperuricemia. gout, or myeloproliferative disorders. Struvite / Infection stones Composed of calcium, ammonium, magnesium phosphate (Triple phosphate stones). Tend to grow in alkaline urine , especially with Proteus infection forming staghorn calculi. Formed in high urinary concentration of ammonia. More common in women (increased susceptibility for UTI). Most stag horn calculi are silent and cause progressive destruction of renal parenchyma. Increased tendency to form struvite calculi is seen in: Foreign body in the urinary tract (Foley's catheter) and Neurogenic bladder/ Bladder dysfunction/Bladder outlet obstruction.

Renal calculi – types Cystine stones Extremely hard stone, formed in acidic urine; Radio-opaque due to double sulphur bonds Occur in cystinuria with typical "ground glass" appearance with a round smooth outline Typical benzene or hexagonal cystine crystals in urine. Xanthine stones Seen in xanthinuria, radiolucent Stones are smooth, brick red colored, round and show lamination on cross section

Renal calculi – types

Renal calculi – investigations

Hydronephrosis Unilateral Hydronephrosis Unilateral hydronephrosis is more common in women and on the right. Mild pain or dull aching in the loin, often with a sensation of dragging heaviness made worse by excessive fluid intake. The kidney may be palpable. Intermittent hydronephrosis (Dietl's crisis) – A swelling in the loin is associated with acute renal pain. Some hours later the pain is relieved and the swelling disappears when a large volume of urine is passed Bilateral Hydronephrosis From lower urinary obstruction symptoms of bladder outflow obstruction predominate. The kidneys are unlikely to be palpable because renal failure intervenes before the kidneys become sufficiently large. Hydronephrosis is an aseptic dilatation of the kidney caused by obstruction to the outflow of urine. There is calyceal dilatation & renal parenchyma is destroyed by pressure atrophy. Diagnosis – Isotope renography (DTPA scan) is the best test.

Adult polycystic kidney disease Inheritance is autosomal dominant Chromosome affected: 16 & 40; Protein abnormality: Polycystin Usually bilateral An important cause of renal failure, accounting for 10-15% of patients who receive haemodialysis. Pathology – Kidneys are grossly enlarged with multiple cysts Cyst are distributed uniformly throughout cortex & medulla Cysts contain straw colored fluid that may become haemorrhagic Renal arteriolar thickening is a prominent finding in adults

Adult polycystic kidney disease – c/f Usually occurs in 3rd or 4th decade. Most Common clinical feature is hypertension (75% adults & 25% children) due to activation of rennin angiotensin system. Pain due to infection (pyelonephritis)/obstruction/sudden haemorrhage. Hematuria, nocturia (due to impaired concentrating ability), nephrolithiasis Progressive decline in renal function leading CRF Most Common cause of death: Cardiovascular disorders Extra-renal manifestations: Cysts are seen in Liver (MC), spleen, pancreas and ovaries.

Adult polycystic kidney disease – dx IVP in ADPKD • Stretching of the calyces by the cysts (spider leg or bell like deformity) • Bubble appearance (calyceal distortion) • Swiss cheese appearance CT scan is investigation of choice in ADPKD

infantile polycystic kidney disease Inheritance is autosomal recessive Usually bilateral If diagnosed at birth, child dies in 2 months due to uraemia and pulmonary hypoplasia Associated with hepatic fibrosis, leading to portal hypertension and hepatic failure; pulmonary fibrosis Diagnosis – IVP: Delayed function with characteristic radial or medullary streaking (sunburst pattern)

Horseshoe kidney Most Common renal fusion abnormality , more common in males Fusion at the lower poles by a parenchymatous or fibrous isthmus Clinical Features – Most are asymptomatic Most Common symptom: vague abdominal pain Rovsing syndrome: abdominal pain, nausea and vomiting on hyperextension of spine Diagnosis: IVP – Flower vase like curves of ureters.

Wilm’s tumour MC primary renal tumor of childhood (2-5 years). 2nd MC malignant abdominal tumor in children (MC is neuroblastoma). MC presenting feature is asymptomatic abdominal mass or swelling. Mostly unilateral . Characterized by triad of abdominal mass, fever & microscopic hematuria. USG (first investigation) or CT abdomen for staging. MRI is superior to other imaging modalities in delineating nephroblastomatosis elements.

bladder In adults, MC type of vesical stone (seen in >50% of cases) is composed of uric acid. MALACOPLAKIA – Inflammatory disease of the bladder that can also affect ureters & kidneys In the bladder, it manifests as plaques or nodules made of large histiocytes (von Hansemann cells) with laminar inclusion bodies (Michaelis-Gutmann bodies) form around bacterial fragments (E. coli) which acts as nidus. Believed to result from the inadequate killing of bacteria by macrophages or monocytes that exhibit defective phago-lysosomal activity.

bladder INTERSTITIAL CYSTITIS / HUNNER’S ULCER Prevalent in women. Ulceration of the mucosa occurs in the fundus of bladder. First symptom – Increased frequency .

Bladder rupture Bladder injuries occur most often from external force to full bladder and often associated with pelvic fractures. Pelvic fracture accompanies bladder rupture in 90% cases. Classic triad suggestive of bladder rupture: Suprapubic pain and tenderness + Difficulty in ability to pass urine + Hematuria. Most Common cause is pelvic fracture. Diagnosed by cystogram or CT cystography. Flame sign or pear sign (pattern of contrast extravasation) or tear drop bladder is seen.

Bladder rupture

SCHISTOSOMIASIS / BILHARZIASIS Schistosomiasis is an infection with Schistosoma haematobium . More common in Males. Man is the only definitive host & intermediate host is snail. MC symptom of urinary schistosomiasis is urinary frequency. Swimmer's itch is the first clinical sign Katayama fever (Acute schistosomiasis) Schistosomiasis is the most common cause of bladder calcification.

Ca urinary bladder

Ca urinary bladder

Ca urinary bladder

Benign prostate hypertrophy BPH develops in the transition zone . It is truly a hyperplastic process. C/F – Obstructive symptoms include – hesitancy decreased force & caliber of stream sensation of incomplete bladder emptying double voiding (urinating a second time within 2 hours of the previous void) straining to urinate & post-void dribbling. Irritative symptoms include frequency, urgency & nocturia (FUN).

Benign prostate hypertrophy

Prostate ca MC cancer of males . MC cause of bone secondaries. Risk factors – Advancing age & Increased fat intake Lycopene, Vitamin A & E and selenium decrease the risk. Pathology - MC type is adenocarcinoma > TCC Prostatic adenocarcinoma are often multifocal & heterogenous Diagnosis of CA prostate based on absence of basal cell layer. Site: Peripheral zone- 75%, Transition zone- 15%, Central zone- 10%

Prostate ca Spread – Hematogenous spread occurs mostly to bone (axial skeleton is MC site with lumbar spine being most frequently implicated) forming osteoblastic secondaries. Visceral metastasis most commonly involve lungs > liver > adrenal glands. Lymphatic metastasis are most often identified in obturator nodes. Diagnosis – Prostate Biopsy. TRUS guided biopsy is done inpatients with abnormal DRE or elevated PSA or both. Differentiation of tumor is graded by Gleason score . A sum of 7 or more suggests an aggressive cancer.

Prostate ca – PSA

hypospadias Hypospadias results when fusion of urethral folds is incomplete, and urethral meatus opens on the underside of penis or perineum (ventral surface of penis). Occurs in 1:250 male births and multifactorial in inheritance. Hypospadias is most common congenital malformation of urethra. Associated Abnormalities – Undescended testis; Inguinal hernia; Urinary tract abnormality

epispadias Urethra opens on the dorsum (upper aspect) of the penis in males, in females there is a fissure in the wall of the urethra which opens above the clitoris Associated Anomalies – Ectopia vesicae; Dorsal Chordee; VUR. Clinical Features – Females: Bifid clitoris & separation of the labia. Males: Patients with glandular epispadias seldom have urinary incontinence.

Posterior urethral valve Symmetrical folds of urothelium extending distally from prostatic urethra to external urinary sphincter. Exclusively an anomaly of male urethra. Clinical Features – Newborns may present with palpable abdominal masses (distended bladder, hydronephrotic kidneys & ascites) Infants with urinary infection & sepsis. Associated with – Oligohydramnios; Pulmonary hypoplasia (MC cause of death.) Investigation of choice – Micturating Cystourethrogram.

phimosis Phimosis is a condition in which the contracted foreskin cannot be retracted over the glans. Chronic infection from poor local hygiene is its most common cause. Most cases occur in uncircumcised males, although excessive skin left after circumcision can become stenotic and cause phimosis. C/F – Difficulty in micturition. Ballooning of prepuce during micturition is suggestive of phimosis. PARAPHIMOSIS – Acquired condition in which the foreskin, once retracted over the glans, cannot be replaced in its normal position. Pathology – Chronic inflammation under the redundant foreskin leads to contracture of preputial opening (phimosis) and of a tight ring of skin when the foreskin is retracted behind the glans.

Phimosis vs paraphimosis

Peyronie’s disease Peyronie's disease (plastic induration of penis/ penile fibromatosis) usually seen over 40 years of age. It is due to fibrous plaques in one or both corpus cavernosum of varying sizes involving tunica albuginea which may later calcify or ossify. Galezia's Triad: (DPR) Dupuytren's contracture + Peyronie's disease + Retroperitoneal fibrosis. C/F - Painful erection, curvature of penis and poor erection distal to involved area. Palpable induration or mass appears usually on the dorsolateral aspect of the penis.

Undescended testis Birth weight may be the principal determinant of UDT at birth and at 1 year of life, independent of the length of gestation. In UDT, 80% are palpable and 20% are nonpalpable. Most common location for an ectopic UDT is within the superficial pouch. Histopathologic hallmark – Decreased numbers of Leydig cells is the earliest abnormality; evident b/w 1-2 years of age Relative risk of testicular tumor is increased 17 times. MC tumor that develops is seminoma . Higher the testis, greater the risk (Abdominal testis has higher risk than inguinal) Orchiopexy does not decrease the risk , it helps in early detection only. Dx – IOC is Inguinal exploration

Testicular torsion Twisting of testis on the spermatic cord, resulting in strangulation of the blood supply and infarction of testis. C/F - Sudden agonizing scrotal pain with nausea or vomiting Absent cremasteric reflux is highly suggestive of torsion testis (present in epididymitis) Prehn's Sign is negative (On elevation f testis, pain relieved in epididymo -orchitis but not in torsion testis) Deming Sign: Affected testis at higher level because of twisting of cord Angel sign : Opposite testis lies horizontally because of present of mesorchium. Dx – Colour Doppler

Testicular torsion

varicocele Dilated & tortuous veins of pampiniform plexus (veins draining testis & epididymis) lying posterior & above the testis Most common surgically correctable cause of male subfertility Etiology - Absent or incompetent valves in the internal spermatic or left testicular vein (MC) and it joins left renal vein at right angles. Clinical Features - Most Common seen in young adults, tall thin men are frequently affected Painless, compressible mass lying posterior and above the testis Bag of worms like feel on palpation in standing position Marked left side predominance (90%)

hydrocele An accumulation of fluid in layers of tunica vaginalis Vaginal hydrocele (MC) – Abnormal accumulation of serous fluid within the tunica vaginalis.

Scrotum: mcq pointers ACUTE EPIDIDYMO-ORCHITIS: Most Common organism causing epididymoorchitis in < 35 and sexually active males: Chlamydia Most Common organism causing epididymoorchitis in children, elderly, homosexuals: E. coli FOURNIER’S GANGRENE: A form of necrotizing fasciitis , with abrupt onset of a rapidly fulminating genital gangrene of idiopathic origin and gangrene up to deep fasciae.

Testicular tumours SEMINOMA MC histological type of testicular tumour: Mixed. MC tumour of testis. MC bilateral primary testicular tumour. Most radiosensitive testicular tumour. YOLK SAC TUMOUR Testicular tumour with best prognosis. MC testicular tumor in infant & children up to 3 years. LEYDIG CELL TUMOUR MC non-germ cell tumours of testis. Reinke crystals are fusiform-shaped cytoplasmic inclusions are pathognomonic for Leydig cells. LYMPHOMA MC testicular tumor in patients > 60 years. MC bilateral testicular tumour. MC secondary testicular tumour.

Lymph nodes affected in ca MC testicular tumor in prepubertal children: Teratoma MC histologic type of testicular lymphoma: Diffuse large B-cell lymphoma Testicular tumour with worst prognosis: Hurricane tumour (Type of choriocarcinoma)
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