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Comprehensive Multisystem Medical Study Notes (GI, Renal, Hematology, Liver/Pancreas, Diabetes, Endocrine)

Gastrointestinal Disorders (GIT) – comprehensive study notes

  • Learning objectives (Week 1, GIT Pathophysiology):

    • Describe disorders that cause digestive tract bleeding (upper and lower)

    • Outline disorders of gastrointestinal (GI) motility

    • Distinguish acute vs chronic gastritis (etiology, progression, prognosis)

    • Compare duodenal vs gastric ulcers and stress ulcers; recognise inflammatory bowel diseases (IBD)

    • Recognise diverticular disease, bowel obstruction, polyps, and colorectal cancer risk

    • Understand GORD/hiatal hernia, gastritis, peptic ulcer disease (PUD), and their management

  • GIT Bleeding – overview of bleeding in the GI tract

    • Any loss of blood into GI lumen is clinically significant; severity depends on rate/volume

    • Anatomical divisions:

    • Upper GIT bleeding: oesophagus, stomach, duodenum

    • Lower GIT bleeding: jejunum, ileum, colon, rectum

    • Haemodynamic indicators: heart rate and blood pressure are key bedside severity markers; early compensation may mask severity via shunting to brain/heart/lungs

    • Consequences of ongoing haemorrhage: increased gut peristalsis with diarrhoea; orthostatic hypotension; hypovolaemic shock if untreated

  • Upper GIT Bleeding (definitions, presentations & causes)

    • Definition: bleeding proximal to the ligament of Treitz (oesophagus to duodenum)

    • Presentations: haematemesis (bright-red or coffee-ground), melaena (black, tarry stools)

    • Major causes: oesophageal varices (portal hypertension due to cirrhosis), peptic ulcers (gastric/duodenal), Mallory–Weiss tears (mucosal tears after severe retching)

    • Differentiation from haemoptysis (blood from respiratory tract)

  • Lower GIT Bleeding

    • Definition: bleeding distal to the ligament of Treitz (jejunum to rectum)

    • Presentation: haematochezia (bright-red or fresh clots per rectum)

    • Common etiologies: inflammatory bowel disease (IBD: ulcerative colitis, Crohn’s), colorectal carcinoma or large polyps, vascular lesions (angiodysplasia, haemorrhoids, diverticular bleeding)

    • Large-volume brisk bleeding at any level can be life-threatening; rapid resuscitation and localisation are essential

  • Pathophysiology & clinical clues to severity

    • Initial sympathetic activation may cause tachycardia; hypotension develops with continued loss

    • Progressive loss leads to reduced preload, reduced cardiac output, metabolic acidosis, multi-organ dysfunction

  • GIT Motility – general notes

    • Motility disorders disrupt coordination of smooth muscle contraction, sphincter tone, and intraluminal pressure

    • High-yield entities: gastro-oesophageal reflux (GER/GERD) and hiatal hernia

  • Gastro-oesophageal reflux disease (GORD/GERD)

    • Definitions:

    • GOR: retrograde movement of gastric contents into the oesophagus

    • GORD/GERD: chronic pathologic reflux (>2× per week) with mucosal damage or troublesome symptoms

    • Predisposing factors:

    • ↓ lower oesophageal sphincter (LOS) tone or ↑ intra-abdominal pressure

    • Obesity, late-term pregnancy

    • Dietary triggers: alcohol, caffeine, chocolate, spicy/fatty foods, peppermint

    • Drugs: anticholinergics, nitrates, CCBs, nicotine

    • Hiatal hernia (see below) disrupts LOS integrity

    • Pathophysiology: acid chyme exposure damages distal oesophageal mucosa; bile salts/pancreatic enzymes amplify injury; chronic exposure → oesophagitis, ulcers, Barrett’s oesophagus (premalignant) → oesophageal adenocarcinoma risk

    • Clinical presentation: heartburn, dysphagia/odynophagia, acid regurgitation, water-brash; atypical features include chronic cough, laryngitis, asthma exacerbation, dental erosion

    • Management (brief outline): lifestyle changes (weight loss, small meals, elevate head of bed), pharmacologic acid suppression (PPIs, H2 antagonists, antacids, prokinetics), refractory cases may require anti-reflux surgery (Nissen/Toupet fundoplication) or endoscopic therapies

  • Hiatal (Hiatus) Hernia – anatomy, types, and management

    • Definition: stomach protrudes through diaphragmatic hiatus into thorax

    • Types:

    • Type I Sliding: gastro-oesophageal junction slides upward; worsened by recumbency, Valsalva, coughing

    • Type II Para-oesophageal (rolling): gastric fundus herniates with junction below diaphragm; risk of strangulation

    • Etiology & risk factors: congenital short oesophagus; repetitive increases in intra-abdominal pressure (COPD, heavy lifting, pregnancy, obesity)

    • Clinical features: often asymptomatic; when symptomatic: reflux, epigastric pain, fullness, dysphagia, occult bleeding/iron deficiency

    • Management: similar to GORD; para-oesophageal hernias often require surgical repair due to volvulus/strangulation risk

  • Gastritis – inflammation of gastric mucosa

    • Classification by time-course: Acute vs Chronic

    • Acute gastritis: rapid onset with barrier failure → surface epithelial necrosis/erosions

    • Common precipitants: NSAIDs, aspirin (inhibit prostaglandin-mediated mucus/bicarbonate), alcohol, smoking, severe physiologic stress (Curling’s ulcers in trauma/sepsis; Cushing’s ulcers with CNS injury via vagal stimulation)

    • Clinical spectrum: dyspepsia, epigastric pain, N/V, bloating; may be asymptomatic with occult bleeding causing iron-deficiency anemia

    • Chronic gastritis: insidious inflammation → atrophy, intestinal metaplasia, dysplasia risk; major categories/causes:

    • Type A (autoimmune) – antibodies to parietal cells and intrinsic factor → hypochlorhydria & pernicious anemia (B12 malabsorption)

    • Type B (bacterial) – chronic Helicobacter pylori infection

    • Chemical/toxic (bile reflux, chronic NSAID, alcohol)

    • Key contrasts: onset, depth of injury, reversibility, immune mechanisms

    • Integrative notes: GORD, hiatal hernia, obesity can form vicious cycles with gastritis and Barrett’s esophagus risk; occult GIT bleeding should prompt endoscopy/colonoscopy in unexplained iron deficiency anemia

  • Peptic Ulcer Disease (PUD) – gastric, duodenal, stress ulcers

    • Definition: loss of protective mucosal barrier → acid/pepsin damage mucosa

    • Classification (non-exclusive): by site (gastric, duodenal, stress ulcers); by time course (acute vs chronic); by depth (erosions vs true ulcers)

    • Gastric ulcers: pain worsens soon after meals

    • Duodenal ulcers: pain relieved by food, typically nocturnal or fasting pain

    • Stress ulcers: shallow ulcers from severe illness/trauma/surgery, catecholamine surge, mucosal ischemia

    • Complications: hemorrhage, perforation with chemical peritonitis, stenosis from scarring

    • Management principles: eradicate H. pylori if present (clarithromycin-amoxicillin-PPI triple therapy; e.g., Nexium Hp7: omeprazole 20 mg bid, amoxicillin 1000 mg bid, clarithromycin 500 mg bid for 7 days), acid suppression (PPIs, H2 antagonists), endoscopic/surgical intervention for active bleeding or perforation, lifestyle changes

    • Historical note: H. pylori established as major etiological agent (Marshall/Warren); Koch’s postulates; Nobel Prize recognition

    • Major pharmacology: PPIs, H2 antagonists, cytoprotectives (sucralfate, misoprostol), antacids

  • Intestinal Obstruction & Bowel Pathologies

    • Intestinal obstruction: impediment to chyme propulsion; mechanical vs functional (paralytic ileus)

    • Mechanical causes: hernia, intussusception, volvulus, adhesions; clinical signs include colicky pain, vomiting, distension, altered bowel sounds; urgent management if signs of strangulation

    • Diverticular disease: diverticulum as mucosal outpouching; risk with low-fiber diet; diverticulosis vs diverticulitis; clinical picture includes LLQ pain, fever, leukocytosis; complications include fistulae, abscess, perforation

    • Inflammatory Bowel Disease (IBD): umbrella for Ulcerative Colitis (UC) and Crohn’s Disease (CD)

    • Shared features: idiopathic, multifactorial; chronic relapsing-remitting pattern; extraintestinal manifestations; increased colorectal cancer risk with duration/extent

    • UC: continuous mucosal/submucosal inflammation starting from rectum; colon-limited; bloody diarrhea, urgency, tenesmus

    • CD: transmural inflammation with skip lesions; any GI segment; could have fistulas, strictures; granulomas; creeping fat; malabsorption

    • Comparative summary: UC vs CD (board-style) – continuous colitis vs transmural, mucosal vs transmural involvement, bleeding in UC, fistulas/strictures in CD, cancer risk patterns

    • Gastrointestinal malignancies (esophagus, stomach, bowel):

    • Esophageal cancer: risk factors include tobacco, alcohol, Barrett’s esophagus; progressive dysphagia

    • Gastric cancer: key risk factors include H. pylori, nitrosamines, high-salt diets; often asymptomatic early

    • Colorectal cancer: second leading cancer death in Australia; adenoma-carcinoma sequence; APC mutations in FAP; metastasis via portal system to liver; early occult bleeding

    • Diagnostic and management themes (GI):

    • Endoscopy (gastroscopy, colonoscopy) with biopsy for diagnosis; bowel prep regimens

    • Imaging: US, CT, MRI, PET; contrast studies for upper/lower GI

    • Stomas: ileostomy/colostomy as needed for management of CRC, obstruction, or IBD; stoma care and pouch systems

  • Take-home concepts & integrative notes

    • Protective mucous-bicarbonate barrier and prostaglandin-mediated mucosal blood flow preserve gastric integrity; NSAIDs impair prostaglandin synthesis → ulcer risk

    • Law of Laplace in diverticulosis: small radius increases luminal pressure, contributing to mucosal herniation at vasa recta points

    • Stress ulcers and intestinal strangulation highlight the importance of prompt hemodynamic resuscitation in critical illness

    • IBD features include extraintestinal autoimmune associations (arthritis, PSC, skin and eye involvement)

    • Endoscopy/colonoscopy play central roles in diagnosis, risk stratification, and surveillance for premalignant polyps and CRC

  • Quick reference numbers & clinical pearls (GI)

    • 50% of cirrhotic deaths linked to bleeding oesophageal varices

    • Orthostatic BP drop > 20 mmHg systolic suggests ≥15% blood volume loss

    • H. pylori prevalence ~50% globally; lifetime peptic ulcer risk in infected individuals ~10–20%

    • Barrett’s oesophagus screening recommended in chronic GORD, especially in males >50 with central obesity

    • Stances on bleeding: upper vs lower GI bleeding localize with endoscopy; rapid resuscitation to reduce mortality

  • Brief notes on GI testing modalities used in nursing practice

    • Endoscopy: pre-procedure fasting (gastric ≥6 h; colon prep with laxatives); monitoring for complications (perforation, bleeding)

    • 24-h pH monitoring; oesophageal manometry for reflux assessment; stool tests (occult blood, pathogens, fat) and breath tests (e.g., 13C-urea for H. pylori)

    • Imaging chain: US, CT, MRI; contrast studies for GI tract

  • Summary takeaway for GI module

    • A broad but interconnected set of disorders—from acid-related injuries and inflammatory diseases to mechanical obstructions and cancers—requires an integrated approach: remove precipitants, control acid or inflammation, restore hemodynamics, surgically intervene when needed, and pursue surveillance (surveillance colonoscopy, Barrett’s screening) to prevent progression and complications.

Renal Disorders – comprehensive notes

  • Objectives (Vid 1 – Pathophysiology):

    • Understand obstructive uropathy pathophysiology

    • Differentiate renal calculi types and their pathophysiology

    • Explain acute tubular necrosis (ATN) pathophysiology

    • Distinguish UTIs and their forms

  • Urinary-Tract Obstruction (Obstructive Uropathy)

    • Definition: any structural/functional hindrance to urine flow; results in impaired flow, collecting-system dilation, ↑ infection risk, compromised renal function

    • Severity determinants: location, duration, unilateral vs bilateral involvement

    • High-level pathophysiology: obstruction → urine backing up → ↑ hydrostatic pressure in renal pelvis; pressures compress tubules/vasculature; sequence of damage: renal tubules → glomeruli; functional decline begins with impaired concentration, then ↓ GFR

    • Upper urinary tract obstruction causes: intraluminal (stones) or extrinsic compression (tumours, retroperitoneal fibrosis, pregnancy uterus)

    • Morphology terms: hydroureter (ureter dilation), hydronephrosis (renal pelvis/calyces dilation)

    • Early detection is critical to prevent irreversible nephron loss

  • Lower Urinary Tract Obstruction

    • Obstruction at bladder neck/outlet or detrusor dysfunction

    • Neurogenic bladder etiologies: stroke, spinal cord injury, MS → loss of voiding reflexes

    • Prostate enlargement (BPH) in aging males → mechanical/dynamic obstruction

    • Other causes: urethral stricture, pelvic organ prolapse, detrusor–sphincter dyssynergia

    • Shared symptoms: flank pain, fever (if infected), nausea/vomiting, edema with renal failure, storage/void symptoms, haematuria

  • Renal Calculi (Nephrolithiasis)

    • Kidney stones: crystalline mineral deposits; pathogenesis multifactorial (supersaturation, low urine volume, urinary pH, loss of inhibitors)

    • Major stone types and features:

    • Calcium stones (75–80%): Ca2+ with oxalate or phosphate; family history risk; middle-aged men

    • Struvite stones (MgNH4PO4): often with recurrent UTIs (Proteus, Pseudomonas); can form staghorn calculi

    • Uric acid stones: persistently acidic urine; associated with gout, leukemia, inflammatory states; radiolucent

    • Clinical presentation: renal colic with sudden severe flank pain radiating to groin; N/V; haematuria; UTIs with fever if infected

    • Diagnostics: non-contrast CT KUB (gold standard), ultrasound, X-ray KUB, urine stone analysis

    • Treatment ladder: hydration and analgesia; ESWL for stones <2 cm; URS + laser lithotripsy; PCNL for large/complex stones

    • Post-procedure nursing: monitor vitals, pain, fluid balance; urine pH management; dietary counseling

  • Acute Tubular Necrosis (ATN)

    • Definition: death of tubular epithelial cells; major intrinsic AKI cause

    • Etiologies: prerenal ischaemia (hypoperfusion) and nephrotoxins (aminoglycosides, radiocontrast, heavy metals, solvents)

    • Triphasic clinical course:

    • Initiation: epithelial injury; ↓ GFR; tubular obstruction by casts

    • Maintenance: ongoing tubular damage; azotemia; fluid overload; hyperkalemia; metabolic acidosis; uremic symptoms

    • Recovery: surviving cells proliferate; polyuric phase with electrolyte losses; gradual Cr/BUN normalization

  • Urinary-Tract Infections (UTIs)

    • Common infections along the urothelium; bacteria often ascend from gut flora (E. coli ~85% of uncomplicated UTIs)

    • Routes: ascending vs haematogenous (less common)

    • Host defenses: glycosaminoglycans in bladder wall, prostatic secretions in men, micturition flushing, ureterovesical junction competence

    • Epidemiology & risk: female sex; pregnancy; menopause; BPH; instrumentation; diabetes; immunosuppression; prior UTIs

    • Cystitis vs Pyelonephritis: cystitis (bladder) vs pyelonephritis (kidneys) – symptoms differ; imaging reserved for atypical/recurrent cases

    • Cystitis features: frequency, urgency, dysuria; suprapubic pain; haematuria; elderly may be asymptomatic or present with confusion

    • Pyelonephritis features: fever, flank pain, costovertebral angle tenderness; may co-occur with cystitis

    • Chronic pyelonephritis: recurrent infection → scarring; potential CKD progression

  • Diagnostic & management pointers for renal disorders

    • Diagnostics: history, urinalysis (dipstick, microscopy), urine culture, imaging (USS, CT), renal function tests (Cr, BUN, eGFR)

    • ATN vs prerenal azotemia: differentiation via fractional excretion of sodium (FENa) – higher in ATN (>2%)

    • Obstruction relief: prompt relief (stent, nephrostomy) can restore function if performed before irreversible cortical atrophy

    • Calculi prevention: hydration targets (urine output >2 L/day), dietary sodium restriction

    • Pregnant patients with asymptomatic bacteriuria require treatment to prevent pyelonephritis

  • Chronic Kidney Disease (CKD) – overview

    • Modern terminology: AKI vs CKD; CKD is a progressive, often irreversible decline in kidney function

    • Causes: diabetes, hypertension (systemic diseases); chronic glomerulonephritis; chronic pyelonephritis; obstructive uropathy; nephrotoxins

    • KDIGO staging by eGFR (mL/min/1.73 m^2) with albuminuria categories A1–A3

    • Stages (eGFR):

    • Stage 1: >90 with kidney damage evidence

    • Stage 2: 60–89

    • Stage 3: 45–59 (3a) or 30–44 (3b)

    • Stage 4: 15–29

    • Stage 5 (ESRD): <15 or dialysis

    • Functional and systemic consequences: ↓EPO → anaemia;↓ urine concentrating ability → polyuria/nocturia; electrolyte and acid-base disturbances; bone-mineral disorders (CKD-MBD); immune dysfunction; risk of cardiovascular disease

    • Diagnostic pearl: urine albumin-to-creatinine ratio; biopsy-proven pathology for staging when necessary

  • CKD progression & systemic sequelae (Integrated perspective)

    • Cardiovascular disease: hypertension, LVH, accelerated atherosclerosis

    • Haematologic: anaemia from ↓EPO; platelet dysfunction

    • CKD-MBD: hyperphosphatemia, secondary hyperparathyroidism, bone disease

    • Acid-base: metabolic acidosis due to reduced acid excretion

    • Endocrine/metabolic: insulin clearance changes; dyslipidemia

    • Immune: uraemia-related immune dysfunction

  • Cross-cutting management concepts in CKD/AKI

    • Early detection and prevention of CKD progression save costs and improve life quality

    • Blood pressure and glycemic control slow progression

    • Renal replacement therapy (RRT) thresholds and dialysis modalities:

    • Haemodialysis (HD)

    • Peritoneal dialysis (PD)

    • Vascular access care and infection prevention; patient education; lifestyle adaptations

  • AKI identification & diagnostics (KDIGO criteria – Stage definitions)

    • Stage 1: Cr rise ≥0.3 mg/dL within 48 h or 1.5–1.9× baseline within 7 days; urine output <0.5 mL/kg/h for 6–12 h

    • Stage 2: Cr 2.0–2.9× baseline; urine output <0.5 mL/kg/h for ≥12 h

    • Stage 3: Cr ≥3× baseline or ≥4 mg/dL or initiation of RRT; urine output <0.3 mL/kg/h for ≥24 h or anuria ≥12 h

    • Pathophysiology frameworks: prerenal (hypoperfusion), intrinsic (parenchymal), postrenal (obstruction)

    • Fluid status management in AKI: euvolemia maintenance vs hypovolaemic resuscitation vs hypervolemia management with diuretics or dialysis as needed

  • Acute kidney injury (AKI) management – quick practical tips

    • Identify reversible factors (sepsis, dehydration, nephrotoxins, obstruction)

    • Support perfusion and avoid further renal insults

    • Monitor electrolytes and acid-base status; manage hyperkalemia via Calcium-Insulin-Glucose-Bicarb-β-agonist-Removal as needed

    • Fluid management strategy: 250–500 mL boluses for hypovolaemia; maintain euvolemia with careful fluid balance

  • Quick numerical references (Renal)

    • Minimum urine output target in AKI: 0.5\text{ mL/kg/h}

    • Normal post-void residual: <30\text{ mL}

    • Dialysis indication: eGFR < 15 mL/min/1.73 m^2

  • Renal Replacement Therapy (RRT) – options

    • Haemodialysis (HD): extracorporeal diffusion/ultrafiltration via fistula/graft or central venous catheter

    • Peritoneal dialysis (PD): peritoneal membrane as semi-permeable barrier; dialysate dwells and drains

  • Nutrition & pharmacology in CKD

    • Nutrition: restrict potassium, sodium, phosphorus; moderate protein intake; energy sufficiency; renal formulas for nutrition support

    • Pharmacology: potassium binders, phosphate binders, bicarbonate for acidosis, EPO-stimulating agents for anemia, iron/folate supplementation when indicated, statins for CV risk

  • Ethical/practical considerations

    • Early recognition/prevention reduces CKD progression and dialysis need

    • Catheter stewardship and infection prevention are critical

    • Polypharmacy risks in older adults; medication reconciliation to avoid nephrotoxins

    • Shared decision-making around dialysis vs conservative care

  • Short-form summary for Renal module

    • Obstruction leads to hydronephrosis; stones are common obstructive lesions

    • ATN arises from ischaemic or nephrotoxic injury

    • UTIs range from cystitis to pyelonephritis; pregnancy and BPH are important risk factors

    • CKD is staged by eGFR and albuminuria; progression leads to ESRD with systemic complications

    • Management emphasizes prevention, hemodynamic optimization, prompt relief of obstruction, and timely dialysis when indicated

Haematology – red blood cells, leukemias/lymphomas, coagulation

  • Core RBC/anaemia concepts

    • Anaemia = reduced oxygen-carrying capacity; often due to ↓Hb or ↓RBC count; MEL (<- measure of Hb content per cell as -cytic/-chromic descriptors)

    • Major anemias covered:

    • Iron-deficiency anaemia (IDA): microcytic, hypochromic; most common worldwide; causes include malnutrition, malabsorption, chronic blood loss; treatments include iron replacement and treating the source

    • Folate deficiency anaemia (megaloblastic): macrocytic; due to inadequate intake or malabsorption; oral folate supplementation

    • Vitamin B12 deficiency anaemia (pernicious anaemia): macrocytic; autoimmune destruction of intrinsic factor/parietal cells; lifelong B12 injections

    • Aplastic (anaplastic) anaemia: pancytopenia; bone marrow failure; transplant as treatment of choice

    • Sickle-cell anaemia (SCA): HbS polymerization under deoxygenation; vaso-occlusive crises; chronic haemolytic anaemia; prone to infections; management includes hydration, pain control, vaccination, transfusions, hydroxyurea in some cases

    • Thalassaemia (α & β): defective globin synthesis; varying severity; management with transfusions and chelation as needed

    • Polycythemia: excess Hb mass; relative (dehydration) vs absolute (primary PV or secondary to hypoxia)

  • Leukaemia – general concepts

    • Definition: malignant proliferation of leukaemic blasts; marrow overcrowding → pancytopenia and impaired blood cell production

    • Classifications depend on cell of origin and differentiation speed:

    • Acute myeloid leukaemia (AML): rapid course; blasts >20% of marrow; myeloid lineage; Auer rods can be present in some variants; risk of tumour lysis syndrome; DIC risk in APL

    • Acute lymphoid leukaemia (ALL): most common childhood cancer; lymphoid blasts; mediastinal mass common in T-ALL

    • Chronic myeloid leukaemia (CML): BCR-ABL1 fusion (Philadelphia chromosome t(9;22)); three-phase course: chronic, accelerated, blast crisis; targeted therapy with tyrosine kinase inhibitors (TIKs)

    • Clinical features: fatigue, infections, bleeding; bone pain; splenomegaly; constitutional B symptoms (fever, night sweats, weight loss)

    • TLS: risk with high turnover; hyperuricaemia, hyperkalaemia, hyperphosphataemia; treat with hydration and allopurinol/rasburicase

  • Lymphomas – general concepts

    • Malignant proliferation of lymphocytes; major groups: Hodgkin’s lymphoma (HL) and Non-Hodgkin’s lymphomas (NHL)

    • HL: Reed–Sternberg cells; bimodal age distribution; typically presents with painless lymphadenopathy and B symptoms; Ann Arbor/Lugano staging; radiotherapy/chemo as standard; prognosis excellent in early stages

    • NHL: diverse B-cell, T-cell, and NK-cell lymphomas; management includes CHOP-like regimens, rituximab (anti-CD20), immunotherapy, targeted therapies, and transplant depending on type/stage

    • Practical points: pancytopenia signs require prompt recognition; fertility/cardiotoxicity with high-dose chemo; access to novel therapies raises cost/inequity considerations

  • Alterations of Platelets and Coagulation

    • Overview: haemostasis requires intact vessels, platelets, and coagulation factors; disorders can lead to bleeding or thrombosis

    • Thrombocytopenia (low platelets)

    • Definition: platelets <150 x 10^9/L; spontaneous bleeding risk lower than when platelet counts drop further (risk significant below 100 x 10^9/L; spontaneous bleeding around 10–15 x 10^9/L; severe bleeding below ~10 x 10^9/L)

    • Causes: decreased production (bone-marrow failure, nutritional deficiencies), increased destruction (ITP, HIT, DIC, infections), sequestration, dilutional effects

    • Clinical signs: petechiae (<3 mm), purpura (0.3–1 cm), ecchymoses (>1 cm)

    • Inherited factor deficiencies – Hemophilias

    • Haemophilia A: Factor VIII deficiency; X-linked; severity defined by FVIII activity

    • Haemophilia B: Factor IX deficiency (Christmas disease)

    • Haemophilia C: Factor XI deficiency (autosomal recessive; often milder)

    • von Willebrand disease (vWD)

    • Heterogeneous group of disorders; VWF deficiency or dysfunction; impairs platelet adhesion and reduces FVIII stability

    • Bleeding tendency is mainly mucocutaneous; prolonged bleeding time and sometimes prolonged aPTT

    • Disseminated Intravascular Coagulation (DIC)

    • Systemic activation of coagulation with widespread microvascular thrombosis and consumption of platelets/factors → bleeding risk

    • Triggers: sepsis (esp. Gram-negative), trauma, obstetric emergencies (abruption, amniotic-fluid embolism), malignancy (APL/malignancies)

    • Laboratory profile: thrombocytopenia, prolonged PT/aPTT, low fibrinogen, elevated D-dimer/FDPs; schistocytes on smear; consumption coagulopathy

    • Management: treat trigger, supportive transfusions (platelets, FFP, cryoprecipitate), careful hemodynamic support; consider low-dose heparin in selected thrombosis-dominant cases

    • Replacement therapy & considerations

    • Replacement factors as needed: FVIII for Hemophilia A, FIX for Hemophilia B, vWF-containing concentrates for vWD, cryoprecipitate for fibrinogen, FFP as needed

    • FEIBA and rFVIIa in inhibitors to factor VIII/IX

    • Nursing & practical considerations

    • Genetic counselling for inherited bleeding disorders

    • Time-sensitive factor replacement; monitor trough levels; RICE for joint bleeds; prophylaxis and safety precautions for minor bleeds

    • Risks of transfusion reactions and allo-immunization; careful product selection

  • Quick reference values & mnemonics

    • Platelet threshold for significant bleeding risk: <30 x 10^9/L (clinical threshold varies by procedure)

    • DIC: low platelets, prolonged PT/aPTT, reduced fibrinogen; elevated D-dimer

    • Hemophilia severities by activity of factor: <1% severe; 1–5% moderate; 5–40% mild

    • Replacement therapy reminders: “time is joint” for joint bleed management; monitor for inhibitors

  • Anticipated exam red flags

    • <20% marrow blasts = not acute leukemia; >20% blasts suggests acute leukemia

    • Philadelphia chromosome suggests CML (or ALL with BCR-ABL fusion)

    • Auer rods plus DIC point toward acute promyelocytic leukemia (APL)

    • Painless lymphadenopathy with B-symptoms should raise lymphoma suspicion

  • Quick clinical links to lab investigations

    • Full blood count (Hb, RBC, WBC, platelets) with indices (MCV, MCH)

    • Coagulation studies: PT/INR, aPTT; bleeding time (historical)

    • Specific factor assays and vWF testing in suspected hemophilia or vWD

  • Ethical/practical notes for Haematology

    • Immunotherapy and targeted therapies (e.g., rituximab, CAR-T) raise cost and access concerns; informed consent essential

    • Genetic counselling is critical for inherited disorders; reproductive choices may be discussed

    • Transfusion strategies should balance clinical benefit with infection risk and resource allocation

Liver, Gallbladder & Pancreas – comprehensive notes

  • Liver disease – overview

    • Major inflammatory liver disorders:

    • Non-Alcoholic Fatty Liver Disease (NAFLD / NASH) – common; linked to obesity and metabolic syndrome; disease spectrum from fatty change to steatohepatitis to cirrhosis

    • Alcoholic Liver Disease (ALD) – fatty liver → alcoholic hepatitis → cirrhosis; progression is linked to alcohol intake

    • Cirrhosis – end-stage fibrosis with regenerative nodules; portal hypertension; multisystem involvement

    • Portal hypertension complications: ascites, esophageal/gastric varices, splenomegaly; management includes diuretics, paracentesis, TIPS, transplant considerations

    • Hepatic encephalopathy – neurotoxic ammonia accumulation in CNS; signs range from subtle cognitive changes to coma

    • Jaundice – due to impaired bilirubin processing/excretion; subtypes include hepatocellular and obstructive

    • Ascites pathophysiology: portal hypertension plus hypoalbuminemia → fluid accumulation; management includes Na+ restriction, diuretics, paracentesis with albumin replacement

    • Hepatic complications: hepatocellular carcinoma risk with chronic viral hepatitis and cirrhosis; variceal surveillance via endoscopy; HCC screening with ultrasound/AFP in cirrhotic patients

  • Viral hepatitis – overview

    • HAV, HBV, HCV, HDV, HEV – transmission routes vary; course ranges from acute to chronic infection; chronic HBV/HCV associated with cirrhosis and hepatocellular carcinoma (HCC)

    • Vaccination and antiviral therapies are central to management (HBV vaccine, DAAs for HCV)

  • NAFLD/NASH and ALD progression

    • Progression model: Alcohol/NAFLD-related steatosis → steatohepatitis → fibrosis → cirrhosis; cessation of alcohol or weight loss can reverse early fatty changes

  • Biliary disorders

    • Cholelithiasis (gallstones)

    • Stone chemistry: cholesterol stones (most common in Western populations) and pigment stones (black/brown; associated with cirrhosis or hemolysis)

    • Pathogenesis: supersaturation of bile with cholesterol or bilirubin; risk factors include female sex, obesity, rapid weight loss, OCPs

    • Clinical features: often asymptomatic; biliary colic postprandial RUQ pain; obstructive signs if CBD involvement with jaundice

    • Management: analgesia; antibiotics if infection; dissolution therapy (UDCA) in select cases; ERCP for CBD stones; cholecystectomy for symptomatic stones

    • Cholecystitis – gallbladder inflammation often due to cystic duct obstruction; Murphy’s sign; management includes antibiotics and cholecystectomy

    • Choledocholithiasis – CBD stones causing obstructive jaundice

  • Pancreas – pancreas disorders

    • Pancreatic dysfunction includes pancreatitis (acute and chronic) and pancreatic cancer

    • Pancreatitis

    • Acute pancreatitis: sudden inflammatory process; common triggers include gallstones and heavy alcohol use; pathophysiology involves ductal obstruction/toxicity → premature activation of pancreatic enzymes → autodigestion; potential for systemic inflammatory response syndrome (SIRS) and MODS

    • Clinical picture: sudden severe epigastric pain radiating to back; N/V; elevated serum lipase/amylase; jaundice if gallstone etiology

    • Chronic pancreatitis: recurrent inflammation → fibrosis; exocrine and endocrine insufficiency leading to steatorrhea and diabetes (type 3c) progression

    • Pancreatic cancer

    • Exocrine ductal adenocarcinoma is most common; high mortality; presents late; risk factors include smoking and chronic pancreatitis

    • Pancreatic/gallbladder management

    • Postoperative care after cholecystectomy; ERCP for ductal obstruction; T-tubes or JP drains when needed; nutritional guidance for post-op recovery

  • Liver/pancreas/gallbladder nursing management pointers

    • Monitor liver function tests (LFTs), bilirubin, albumin, coagulation profile

    • Manage ascites with diuretics and dietary sodium restriction; monitor daily weights and abdominal girth

    • Monitor for hepatic encephalopathy signs; ammonia management (lactulose, rifaximin) if indicated

    • Nutrition: ensure adequate calories; address fat-soluble vitamin deficiencies; protein management depending on CKD or cirrhosis state

    • Postoperative care: wound/drain care after biliary/pancreatic surgery; monitor for bile leaks and infection

  • Key numbers, equations & clinical flow (Liver Pancreas Gallbladder)

    • Portal hypertension threshold: portal vein pressure > 12\text{ mmHg}

    • Ascites: >1500\text{ mL} peritoneal fluid; albumin replacement: 8\text{ g IV albumin per litre of ascitic fluid removed}

    • Bilirubin normal: < 20\text{ micromol/L}; jaundice often evident > 40\text{ micromol/L}

    • Portal hypertension complications: varices, ascites, splenomegaly

    • Pancreatitis markers: lipase/amylase elevation; consider triglycerides for hypertriglyceridemia pancreatitis

    • Post-op and perioperative considerations: go through standard pre/postoperative thyroid surgery parallels for endocrine disorders where relevant; watch for hypocalcemia after parathyroid involvement in thyroid surgery

  • Diagrams in practice (recollection tips)

    • Visualize flow: GIT disorders affect digestion, absorption, and bleeding pathways; CKD/AKI affects filtration and excretion; liver disease impacts detoxification, metabolism, bile production, and portal pressure; pancreatic/gallbladder disorders affect digestion and bile/pancreatic enzyme flow

Endocrine & Thyroid – overview, hyper/hypothyroidism; goitre management

  • Thyroid anatomy & physiology

    • Thyroid gland: two lobes connected by an isthmus; follicular cells secrete T3/T4; parafollicular (C) cells secrete calcitonin

    • Regulation: hypothalamus releases TRH → pituitary releases TSH → thyroid secretes T4/T3; negative feedback restores homeostasis

    • Actions of thyroid hormones: regulate basal metabolic rate, heat production, tissue growth, nervous system development and cardiovascular function; calcitonin lowers serum calcium (minor role in adults)

  • Hyperthyroidism & thyrotoxicosis

    • Hypersecretion of T3/T4; thyrotoxicosis refers to the metabolic effects of excess thyroid hormone

    • Primary hyperthyroidism: thyroid dysfunction; Secondary hyperthyroidism: pituitary overproduction of TSH

    • Graves’ disease: autoimmune TSH receptor-stimulating antibodies; most common cause of hyperthyroidism

    • Clinical features: weight loss with increased appetite; tachycardia; heat intolerance; sweating; tremor; goitre; exophthalmos (Graves’ specific)

    • Diagnosis: TSH, free T4; consider ECG for cardiac effects

    • Management: antithyroid drugs, beta-blockers for symptomatic relief, radioactive iodine therapy, and thyroidectomy in selected cases; dietary caffeine/specific nutrition guidance; pre/postoperative care for thyroid surgery

  • Hypothyroidism

    • Causes: iodine deficiency; Hashimoto thyroiditis (autoimmune destruction of thyroid tissue); congenital hypothyroidism; pituitary/hypothalamic failure (secondary)

    • Signs: fatigue, weight gain, cold intolerance, constipation, bradycardia, goitre

    • Myxedema (severe hypothyroidism): facial edema, thickened features; life-threatening if untreated

    • Management: thyroxine (levothyroxine) replacement with dose titration and monitoring for interactions

  • Goitre & goitrous conditions

    • Goitre: enlarged thyroid; can be non-toxic (iodine deficiency) or toxic (hyperfunction)

    • Pre-/post-operative considerations: preoperative optimization; ensure airway safety; post-op asthma/inhalation precautions; regular monitoring

  • Adverse management & nursing implications

    • Regular thyroid function monitoring during therapy adjustments

    • Educate on medication adherence and recognition of adverse effects

    • Pre- and postoperative planning for thyroid surgery (thyroidectomy) – goals: reduced stress, monitoring for hypocalcemia post-parathyroid involvement, airway protection, voice preservation

  • Summary: Thyroid health integrates with metabolism, growth, and cardiovascular function; Graves’ disease is a top differential for hyperthyroidism; Hashimoto’s is a leading cause of hypothyroidism; congenital hypothyroidism must be treated early to prevent neurodevelopmental deficits

Adrenal Glands – Addison’s disease, Cushing’s syndrome, and adrenal management

  • Adrenal anatomy & hormone regulation

    • Adrenal glands located above kidneys; outer cortex and inner medulla

    • Adrenal cortex zones:

    • Zona glomerulosa → mineralocorticoids (Aldosterone)

    • Zona fasciculata → glucocorticoids (Cortisol)

    • Zona reticularis → gonadocorticoids (androgens)

    • Medulla secretes catecholamines (adrenaline and noradrenaline)

    • Regulation via HPA axis and sympathetic inputs: CRH → ACTH → cortisol; adrenal medulla responds to sympathetic input

    • Key hormones: Cortisol, Aldosterone, Androgens; Catecholamines

  • Cortisol and aldosterone actions

    • Cortisol: stimulates gluconeogenesis, increasing blood glucose; promotes lipolysis and protein breakdown; increases vascular reactivity; immune modulation

    • Aldosterone: promotes Na+ and water reabsorption in kidney; increases K+ excretion; regulates fluid balance and BP

  • Hyposecretion states – Addison’s disease (adrenocortical insufficiency)

    • Causes: autoimmune destruction of adrenal cortex; infections (e.g., TB); adrenal hemorrhage; secondary adrenal insufficiency (low ACTH from pituitary)

    • Pathophysiology: loss of cortisol negative feedback → high ACTH (hyperpigmentation due to POMC/ACTH precursor) – Addison’s syndrome

    • Clinical features: fatigue, weakness, weight loss, anorexia; hyponatremia and salt cravings; hyperkalemia; orthostatic hypotension; hyperpigmentation (adrenal crisis signs)

    • Diagnostic tests: ACTH stimulation test; plasma/urine cortisol; electrolyte disturbances (low Na+, high K+); imaging as needed

    • Management: correct underlying cause; hydrocortisone replacement with stress dosing; fludrocortisone for mineralocorticoid replacement

    • Addisonian crisis: life-threatening; requires high-dose hydrocortisone and aggressive saline/dextrose resuscitation

  • Hypersecretion states – Cushing’s syndrome

    • Causes: endogenous (ACTH-secreting pituitary adenoma—Cushing’s disease; adrenal tumor) or ectopic ACTH secretion; exogenous corticosteroid excess

    • Signs: central (truncal) obesity, moon face, buffalo hump, purple striae; proximal muscle weakness; osteoporosis; hypertension; hirsutism; menstrual irregularities

    • Diagnostics: plasma cortisol, 24-h urine free cortisol, low-dose dexamethasone suppression test, ACTH levels, imaging (CT/MRI)

    • Management: treat source (surgical removal of adenoma, adrenalectomy, or ectopic source); adjust glucocorticoid therapy; monitor for metabolic complications

  • Nursing considerations

    • Acute and chronic management of adrenal disorders; monitor for infection risk; manage electrolyte disturbances; assess blood pressure and signs of hypovolemia or fluid overload

    • Education and safety: wear medical alert bracelet; carry emergency hydrocortisone dosing instructions; plan for stress-dose steroids during illness or surgery

  • Quick synthesis

    • Adrenal disorders disrupt fluid/electrolyte balance, metabolism, immune response, and stress responses; management hinges on hormone replacement or suppression depending on hypo- vs hypersecretion

Quick reference: Quick Revision Tips (integrated across modules)

  • GIT: manage variceal bleeds and ulcer disease with resuscitation, endoscopy, and pharmacologic therapy; monitor for Barrett’s esophagus in chronic reflux

  • Renal: maintain euvolemia; ensure rapid relief of obstruction; monitor for AKI staging per KDIGO; use KHDA-based management in CKD; plan dialysis or transplantation when indicated

  • Haematology: recognize acute leukemia vs lymphoma; manage coagulopathies (DIC, vWD, hemophilias) with targeted replacement and careful transfusion practice

  • Liver/pancreas/gallbladder: monitor for cirrhosis complications (ascites, varices, HE); treat pancreatitis causes; manage biliary disease with surgical and non-surgical options; prioritize nutrition and infection prevention

  • Endocrine: balance thyroid, adrenal, and gonadal functions; monitor for hypo-/hyper-secretion; address long-term complications and surveillance

  • Equations & key numbers (LaTeX)

    • Variceal bleeding contribution: Proportion of upper GI bleeds from variceal sources is significant in cirrhosis (clinical note)

    • Orthostatic BP drop as volume indicator: \text{SBP drop} > 20\text{ mmHg} indicates substantial volume loss

    • KDIGO stages for CKD (GFR only): Stage 1: GFR>90\text{ mL/min/1.73 m}^2; Stage 2: 60-89; Stage 3a: 45-59; Stage 3b: 30-44; Stage 4: 15-29; Stage 5: <15 or dialysis

    • Albuminuria categories: A1 (normal), A2 (micro), A3 (macro)

    • AKI criteria: \frac{\text{Cr}\text{t1} - \text{Cr}\text{t0}}{\text{Cr}_{\text{t0}}}\text{ criterion} \ \rightarrow \text{≥0.3 mg/dL rise in 48 h}

    • DKA criteria: arterial pH < 7.3; bicarbonate < 15\text{ mmol/L}; presence of ketones

    • Hyperkalaemia management mnemonic: “Calcium–Insulin–Glucose–Bicarb–(β-agonist)–Remove”

    • Diabetes thresholds: HbA1c \text{≥ }6.5\text{ } \ \text{Fasting glucose}\text{ ≥ }7.0\text{ mmol/L}; OGTT ≥ 11.1\text{ mmol/L} (2-hr) for diagnosis

  • Study-scaffold tips

    • Learn major contrasts: UC vs CD; PUD vs gastritis; AKI vs CKD; Type 1 vs Type 2 DM

    • Remember high-yield clinical signs: Jaundice, ascites, oesophageal varices, Barrett’s esophagus, Murphy sign, RBC and WBC changes

    • Use bullet-point summaries per organ system; incorporate diagnostic tests, typical presentations, and first-line managements

    • Practice common pharmacology regimens (e.g., H. pylori triple therapy, PPI/H2 blocker choices, insulin regimens, CKD management medications)

If you would like, I can tailor these notes to specific exam topics or convert this into a printable study sheet with a more compact or more detailed format. Also tell me if you’d prefer