MSC - F. Surgery Answers 2025
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7. Persistent Abdominal Aorta Pulsation
oUnlike other acute abdominal conditions, pulsation in the epigastrium does not abruptly disappear because of edema in retroperitoneal tissues.
8.Tenderness in Left Vertebrocostal Angle
oMayo-Robinson’s symptom, indicating irritation near the pancreas.
9.Left-sided Phrenic Nerve Irritation
oCausing referred pain and respiratory symptoms.
10.Signs of Pancreatogenic Peritonitis
oPeritoneal irritation signs with hypoperistalsis or absence of bowel sounds.
o Presence of free fluid in the abdomen.
11.Respiratory Disturbances
oDyspnea, pleuritis, and atelectasis due to diaphragmatic irritation and systemic inflammatory response.
12.Hemodynamic and Microcirculatory Disorders Leading to Shock
a.Hypotension (decreased blood pressure)
b.Halsted’s sign: cyanosis of anterior abdominal wall
c.Kulen’s sign: periumbilical cyanosis
d.Gray-Turner’s sign: cyanosis/ecchymosis of lateral abdominal walls
e.Mondor’s sign: violet spots on face and body
f.Grunwald’s sign: periumbilical ecchymosis
oThese signs reflect retroperitoneal hemorrhage and enzymatic tissue destruction.
13.Fever
o Usually subfebrile (37.5–38°C), less commonly high fever.
14.Oliguria / Reduced Diuresis
o Due to hypovolemia, shock, and renal hypoperfusion.
6. Complications of acute pancreatitis. Brief description, clinic.
Complications of Acute Pancreatitis
A.Toxemic:
Pancreatogenic shock
ARDS (“pancreatic lung”)
Toxic renal injury
Encephalopathy or delirium
Hemorrhagic erosive gastritis
Pancreatogenic coma
B.Postnecrotic:
1.Degenerative:
Parapancreatic infiltration
Pancreatic pseudocyst
2.Purulent:
Pancreatic abscess
Phlegmonous pancreatitis
Peritonitis
Retroperitoneal phlegmon/abscess
3.Visceral:
Internal/external fistulas (pancreatic, biliary, duodenal, pleural)
Arrosive hemorrhage
Vascular occlusion (portal vein thrombosis, arterial compression)
7. Diagnosis of acute pancreatitis.
Diagnostic Approach
1.Laboratory Tests:
Serum Amylase: Elevated in >90% cases but can normalize or decrease in late destructive stages (a poor prognostic sign).
Urine Diastase: Increased activity supports diagnosis.
Serum Lipase: More specific than amylase, but not elevated in all cases.
Complete blood count: Leukocytosis, hemoconcentration.
Blood glucose: May be elevated due to pancreatic islet cell dysfunction.
Other tests: Liver function tests, coagulation profile, electrolytes, renal function tests.
2.Imaging:
Ultrasound: Pancreatic enlargement, hypoechoic areas suggestive of edema or necrosis, peripancreatic fluid collections. Useful for biliary pathology detection.
CT scan (Contrast-enhanced): Gold standard for staging pancreatitis severity, detecting necrosis, hemorrhage, fluid collections, and complications.
X-ray: Limited value; may show indirect signs (e.g., sentinel loop, colon dilation) or diaphragmatic elevation. Selective angiography useful in specific vascular complications.
Laparoscopy: Used in complicated or uncertain cases; allows direct visualization of hemorrhagic effusions, necrosis, and fat necrosis on peritoneal surfaces.
3.Other Studies:
Fibrogastroscopy: Detects indirect signs such as hemorrhagic gastritis or duodenitis, duodenal mucosal edema, and papillitis.
Differential diagnosis includes perforated ulcers, acute cholecystitis, mesenteric thrombosis, biliary colic, myocardial infarction, and appendicitis.
8. Modern pathogenetic, complex, conservative therapy of acute pancreatitis.
Pathogenetic Complex Conservative Therapy of Acute Pancreatitis
1. Inhibition of Pancreatic Secretion
o Strict bed rest and complete starvation (NPO 3–5 days) o Nasogastric aspiration and intragastric hypothermia
o Atropine (to reduce parasympathetic stimulation)
oOctreotide (Sandostatin) IV — somatostatin analogue to inhibit enzyme secretion
oCytostatic agents (rarely used): 5-fluorouracil (Ftoraur),
Azathioprine
2.Pain Control
oNovocaine (procaine) nerve blocks (paraneural, hepatic ligament block)
o Spasmolytics: e.g., Drotaverine, Papaverine
oAnalgesics: Non-narcotics preferred; narcotics excluding morphine (e.g., Tramadol, Fentanyl)
3.Antienzymatic Therapy
oProtease inhibitors: Contrykal (Aprotinin), Gordox (Gabexate mesilate)
oKallikrein-kinin system inhibitors: Aminocaproic acid, Amidopyrine, Methyluracil
4.Correction of Fluid-Electrolyte and Metabolic Disturbances
oRinger-Lactate solution, Glucose solution
oElectrolyte and acid-base balance correction
5.Improvement of Microcirculation
oRheopoliglyukin (Dextran)
o Trental (Pentoxifylline)
oHeparin (low dose, cautiously)
6.Detoxification
o Haemodesum, Plasmapheresis, Hemosorption
oLymphatic drainage (selective cases)
7.Antimicrobial Therapy
oCombination of Aminoglycosides + Semisynthetic penicillins (e.g., Ampicillin-sulbactam)
9.Surgical treatment of acute pancreatitis. Indications, modern principles and methods of surgical treatment.
Indications for Surgery
1. Early operations (within first hours to days):
o Indicated in cases of pancreatic or pancreatogenic peritonitis,
o Ineffective conservative treatment after 24–48 hours,
o Persistent pain syndrome,
o Progressive intoxication,
oJaundice or signs of peritonitis.
2.Delayed operations:
oPerformed for pyonecrotic complications (infected necrosis, abscess formation) once necrosis is demarcated.
3.Late (elective) operations:
oAfter inflammation subsides, for removal or correction of underlying causes (e.g., biliary obstruction, chronic pancreatitis, or other gastrointestinal diseases predisposing to recurrent attacks).
Modern Surgical Principles and Methods
Surgery aims to treat pancreatic inflammation, manage pancreatogenic peritonitis, prevent or treat toxic complications, and handle postnecrotic complications.
Current surgical approaches are divided into two broad categories:
1.Organ-preserving techniques:
o Capsulotomy: Opening pancreatic capsule to relieve pressure.
oMarsupialization and tamponing of the omental bursa (to drain necrotic fluid).
oDrainage of the omental bursa and peripancreatic spaces:
Facilitates local infusion and active aspiration of enzymes and toxins.
oOmentopancreatopexy: Mobilization of omentum to pancreas to aid healing.
oAbdominization of pancreas: Exposing pancreas to the abdominal cavity for drainage.
2.Resection techniques:
oStage-like sequestrectomy and necrosectomy: Sequential removal of necrotic tissue.
oPartial or total pancreatectomy: Reserved for extensive pancreatic destruction.
oPancreaticoduodenal resection (Whipple procedure): For complex cases involving the head of pancreas and duodenum.
Outcome and Mortality
The outcome ranges from full recovery to progression into chronic pancreatitis.
Mortality rates vary from 7% to 30%, depending on disease severity and timeliness of intervention.
Diseases of the thyroid gland
1. Diagnosis of the thyroid gland diseases.
1.Clinical History and Physical Examination
Detailed anamnesis:
oPay attention to patient's residence (iodine-deficient areas), family history of goiter or thyroid disease.
General appearance:
oFacial expression, eye changes (exophthalmos), finger tremor—may suggest thyroid dysfunction even without visible neck changes.
Neck examination:
oInspect for deformities, goiter size and symmetry, visible veins, pulsations.
oPalpate thyroid gland for size, consistency, nodularity (diffuse, nodular, or mixed), tenderness, mobility, and adherence to surrounding tissues.
Skin assessment:
oNote color, moisture, subcutaneous edema, nutritional status (cachexia or obesity).
2.Laboratory Tests
Serum thyroid hormones:
oTotal T4 (normal: 4.5–11 µg/dL), Total T3 (normal: 100–160 ng/dL).
oFree T4 (normal: 10–30 pmol/L) and Free T3 (normal: 3.5–6 pmol/L) are more clinically relevant as they represent active hormone fractions.
oElevated T3 with normal T4 suggests T3-toxicosis.
Serum Thyroid Stimulating Hormone (TSH):
oMeasured by immunoassay. Normal range ~0.5–5 mU/L.
o Elevated in primary hypothyroidism (can exceed 40 mU/L).
o Suppressed or undetectable in hyperthyroidism.
oSensitive marker for hypothyroidism and monitoring post-treatment.
3.Imaging Studies
Ultrasound (US) of thyroid:
oFirst-line, non-invasive imaging to assess gland size, internal architecture, and nodularity.
X-ray and tomography:
oIndicated for substernal or retrosternal goiter.
oEvaluates size, location, tracheal or esophageal displacement or compression, critical for surgical planning.
Thyroid scintigraphy:
oUses radioactive iodine (I-131) or technetium (Tc-99m).
o Assesses gland size, shape, and functional activity.
oDetects "hot" (hyperfunctioning) and "cold" (hypofunctioning) nodules, ectopic thyroid tissue, and metastases.
4.Functional Tests
Radioactive iodine uptake (RAIU):
oMeasures thyroid iodine absorption at 6, 24, and 48 hours.
o Normal 24-hour uptake: 7–30%.
oIncreased uptake suggests hyperthyroidism; decreased uptake suggests thyroiditis or iodine overload.
Thermovision:
oInfrared thermography as indirect assessment of gland function by measuring temperature over the thyroid.
5.Cytological Examination
Fine-needle aspiration biopsy (FNAB):
oIndicated for morphological evaluation, particularly in nodular thyroid disease.
oHelps differentiate benign from malignant lesions and guides therapeutic decisions.
2.Goiter. Definition, classification.
Definition:
Goiter is an enlargement of the thyroid gland, regardless of its cause or functional state.
Classification:
1. By Etiology:
oEndemic Goiter: Due to iodine deficiency in a specific geographic region (≥5% in children or ≥30% in adults).
oSporadic Goiter: Occurs outside endemic regions; etiology often unclear.
oAutoimmune Goiter:
Hashimoto’s Thyroiditis – Chronic lymphocytic thyroiditis.
Riedel’s Thyroiditis – Fibrous replacement of thyroid tissue.
oToxic Goiter:
Diffuse Toxic Goiter (Graves’ Disease)
Toxic Nodular Goiter
Toxic Adenoma
2.By Morphology:
oDiffuse
o Nodular
oMixed (Multinodular)
3.By Functional Status:
oEuthyroid Goiter – Normal thyroid function.
oHyperthyroid (Toxic) Goiter – Increased thyroid hormone production.
oHypothyroid Goiter – Reduced thyroid hormone production.
4.By Anatomical Location:
o Cervical
o Retrosternal
o Posterior-esophageal
o Sublingual
oAberrant (ectopic thyroid tissue)
5.By Degree of Enlargement (WHO):
oGrade 0 – Not palpable or visible.
o Grade 1 – Palpable, not visible. o Grade 2 – Palpable and visible.
o(Extended: Grades III–V – progressively larger and causing compression symptoms)
3.Endemic goiter. Etiopathogenesis, clinical picture, prevention.
Endemic Goiter (Zob endemicus, Euthyroid goiter):
Definition:
Chronic, non-toxic enlargement of the thyroid gland due to insufficient iodine intake, typically seen in certain geographic regions (≥10% population prevalence).
Function remains euthyroid in most cases.
Etiopathogenesis (in brief):
Primary cause: Iodine deficiency → ↓ T4 → ↑ TSH → compensatory thyroid hypertrophy/hyperplasia.
Hormonal adaptation: Preferential synthesis of T3 over T4 due to lower iodine demand.
Structural evolution:
Compensatory hypertrophy → hyperplasia → microfollicle formation → nodularity (if persistent).
Contributing factors: