from reportlab.lib import colors
from reportlab.lib.enums import TA_CENTER
from reportlab.lib.pagesizes import A4
from reportlab.lib.styles import getSampleStyleSheet, ParagraphStyle
from reportlab.lib.units import cm
from reportlab.platypus import SimpleDocTemplate, Paragraph, Spacer, PageBreak, KeepTogether
from reportlab.pdfbase.pdfmetrics import stringWidth
from reportlab.pdfbase.ttfonts import TTFont
from reportlab.pdfbase import pdfmetrics
from reportlab.lib.colors import HexColor
from reportlab.pdfgen.canvas import Canvas

OUT='/tmp/workspace/git_exam_answers/output/GIT_Complete_Exam_Answers.pdf'

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class NumberedCanvas(Canvas):
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    def showPage(self):
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    def save(self):
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def P(text, style='Bodyx'): return Paragraph(text, styles[style])
def H(text, level=2): return Paragraph(text, styles['H1x' if level==1 else 'H2x'])
def bullets(items): return P('<br/>'.join('• '+x for x in items))

story=[]
story += [P('GASTROINTESTINAL TRACT PHYSIOLOGY','Title2'), P('Complete Exam-Answer Booklet based on the two uploaded question-bank images','SubTitle'), P('<b>Use:</b> Concise, structured answers suitable for short notes, explain-why questions, brief notes and the clinical case. Terms and treatment choices are educational and not a substitute for individual patient care.','Box'), H('Contents',1)]
for x in ['I. Short notes (11)','II. Explain why (6)','III. Explain briefly (11)','IV. Applied question: phototherapy','V. Clinical case question','References and revision points']:
    story.append(P(x))
story.append(PageBreak())

# I
story.append(H('I. Short Notes',1))
short=[
('1. Law of the gut',"The <b>law of the gut</b> states that when a segment of intestine is distended, the peristaltic reflex produces contraction on the oral side and relaxation on the anal side. Hence the wave normally moves aborally, toward the anus. It is coordinated mainly by the myenteric plexus: excitatory cholinergic neurons contract circular muscle behind the bolus, while inhibitory neurons (nitric oxide/VIP) relax bowel ahead of it. This arrangement propels contents in the normal direction."),
('2. Secretion of HCl by the stomach',"HCl is secreted by parietal (oxyntic) cells of the fundus and body. It creates a very acidic gastric lumen (about pH 1-3), converts pepsinogen to pepsin, denatures proteins, kills many ingested organisms and helps release dietary iron. Main stimulants are acetylcholine (vagus), gastrin and histamine; inhibitors include somatostatin, prostaglandins, secretin and low duodenal pH."),
('3. Functions of saliva',"Saliva lubricates oral mucosa and food to aid speech, mastication, swallowing and taste. Its alpha-amylase begins starch digestion and lingual lipase contributes to lipid digestion. Bicarbonate buffers acids; water dissolves tastants; mucus protects mucosa. Antimicrobial actions include flushing plus IgA, lysozyme and lactoferrin. It also protects teeth by buffering acid and providing calcium/phosphate for remineralization."),
('4. Gastric emptying',"Gastric emptying transfers chyme into the duodenum. Antral peristaltic waves grind solids against the closed pylorus (retropulsion); only particles sufficiently small pass through the pylorus. Gastric distension and gastrin modestly promote emptying. Duodenal feedback is dominant: acid, fat, hyperosmolar chyme and distension activate enterogastric neural reflexes and hormones, especially CCK and secretin, reducing antral pump activity and increasing pyloric resistance. Liquids empty faster than solids; fat-rich meals are slowest."),
('5. Segmentation contraction',"Segmentation consists of rhythmic, localized contractions of circular muscle at alternating sites, especially in the small intestine. It repeatedly divides and recombines chyme, mixing it with pancreatic juice, bile and intestinal secretions and bringing it into contact with mucosa for absorption. It produces little net forward movement. Its frequency follows the slow-wave rhythm and is reduced by sympathetic activity."),
('6. Phases of gastric secretion',"<b>Cephalic phase (about 30%)</b>: sight, smell, taste, chewing and thought of food activate the vagus. ACh stimulates parietal and chief cells; vagal GRP stimulates G cells to release gastrin. <b>Gastric phase (about 60%)</b>: stomach distension evokes vagovagal/local reflexes and peptides/amino acids stimulate gastrin, producing the largest acid output. <b>Intestinal phase (about 10%)</b>: small amounts of intestinal gastrin may stimulate initially; subsequently acid, fat and hypertonicity in duodenum inhibit secretion through secretin, CCK, GIP and enterogastric reflexes."),
('7. Movements of the small intestine',"During feeding, segmentation mixes chyme and short peristaltic waves propel it slowly. Peristalsis causes contraction behind and relaxation ahead of a bolus. After fasting, the migrating motor complex (MMC), promoted by motilin, sweeps residual material from stomach through small bowel every 90-120 minutes. The ileogastric/ileal brake slows transit when distal ileum is distended or receives nutrients; the ileocecal sphincter regulates entry into colon."),
('8. Functions of the liver',"The liver forms and secretes bile; conjugates and excretes bilirubin; metabolizes carbohydrates (glycogenesis, glycogenolysis, gluconeogenesis), lipids and amino acids; converts ammonia to urea; and synthesizes albumin, clotting factors and many plasma proteins. It detoxifies/inactivates drugs, alcohol, hormones and toxins; stores glycogen, iron, copper and vitamins A, D, B12 and K; acts in immune clearance through Kupffer cells; and serves as a blood reservoir."),
('9. Mechanism of formation of HCl',"Inside a parietal cell, CO2 + H2O form carbonic acid via carbonic anhydrase; it dissociates to H+ and HCO3-. The apical H+/K+-ATPase pumps H+ into the canaliculus in exchange for K+, while K+ recycles through apical channels. Chloride enters the cell basolaterally in exchange for HCO3- and exits apically through Cl- channels. Luminal H+ and Cl- form HCl. Bicarbonate enters blood after meals, producing the alkaline tide. Water follows osmotically."),
('10. Regulation of gastric juice secretion',"Parietal cells are stimulated synergistically by ACh at M3 receptors, gastrin at CCK-B receptors and histamine at H2 receptors. ACh and gastrin increase intracellular Ca2+; histamine increases cAMP, so combined stimulation is powerful. Gastrin also stimulates ECL-cell histamine release. Acid in the antrum activates D-cell somatostatin, which inhibits G cells, ECL cells and parietal cells. Duodenal acid/fat evoke secretin, CCK and neural enterogastric inhibition. Prostaglandins reduce acid and enhance mucus-bicarbonate protection."),
('11. Pathophysiology of jaundice',"Jaundice is yellow discoloration from raised bilirubin. <b>Prehepatic (hemolytic)</b>: excessive RBC breakdown increases unconjugated bilirubin; urine bilirubin is absent, urobilinogen rises. <b>Hepatocellular</b>: impaired uptake, conjugation and/or secretion by hepatocytes causes mixed unconjugated and conjugated hyperbilirubinemia, often with elevated AST/ALT. <b>Posthepatic/cholestatic</b>: obstruction prevents bile drainage; conjugated bilirubin refluxes into blood and urine, stools become pale, urine dark, pruritus occurs from retained bile salts and ALP/GGT are high.")]
for title,body in short: story += [H(title),P(body)]

story.append(PageBreak()); story.append(H('II. Explain Why',1))
why=[
('1. Achlorhydria is associated with iron-deficiency anemia',"Non-heme dietary iron is absorbed best in the ferrous (Fe2+) form. Gastric HCl solubilizes iron and promotes reduction of ferric (Fe3+) to ferrous iron, making it available for duodenal absorption. In achlorhydria, iron remains less soluble and absorption falls. Atrophic gastritis can also cause chronic mucosal disease or occult blood loss, further contributing to iron deficiency."),
('2. Proton-pump inhibitors are used for gastric ulcers of various etiologies',"PPIs irreversibly inhibit the final common pathway of acid secretion, the parietal-cell H+/K+-ATPase. Therefore they suppress acid regardless of whether stimulation is vagal, histaminergic or gastrin-mediated. Raising intragastric pH relieves acid injury, promotes clot stability in bleeding ulcers and permits mucosal healing. The underlying cause must also be addressed: eradicate H. pylori, stop NSAIDs where possible, and exclude malignancy in a gastric ulcer."),
('3. A protein-rich, low-carbohydrate meal does not cause hypoglycemia',"Amino acids stimulate both insulin and glucagon secretion. Insulin promotes uptake and use of amino acids, while glucagon maintains hepatic glucose output through glycogenolysis and gluconeogenesis. The glucagon response counterbalances insulin, so plasma glucose does not fall markedly despite little dietary carbohydrate."),
('4. CCK has gastrin-like properties',"Gastrin and CCK have similar C-terminal amino-acid sequences and can act at the CCK-B (gastrin) receptor. Thus CCK can weakly stimulate gastric acid secretion and trophic effects at high concentrations. However, its dominant physiological actions are gallbladder contraction, pancreatic enzyme secretion, relaxation of the sphincter of Oddi and slowing of gastric emptying via CCK-A receptors."),
('5. Postprandial alkaline tide occurs',"When parietal cells generate H+ for luminal HCl, they simultaneously generate HCO3-. This bicarbonate exits the basolateral membrane into blood in exchange for chloride. Hence venous blood draining the stomach becomes transiently more alkaline after a meal, and urine may become relatively alkaline."),
('6. Alcohol intoxication is reduced when alcohol is taken after a fat-rich diet',"Fat delays gastric emptying, so alcohol reaches the small intestine, the major site of rapid absorption, more slowly. Food also dilutes alcohol and may increase first-pass gastric metabolism. Consequently the peak blood alcohol concentration rises more slowly and is generally lower than after drinking on an empty stomach. This does not make drinking safe or prevent impairment.")]
for t,b in why: story += [H(t),P(b)]

story.append(PageBreak()); story.append(H('III. Explain Briefly',1))
brief=[
('1. Dietary fibres',"Dietary fibre is nondigestible carbohydrate and lignin from plants. <b>Insoluble fibre</b> (bran, cellulose) increases stool bulk and speeds colonic transit. <b>Soluble, viscous fibre</b> (oats, legumes, pectin) forms gels, slows glucose absorption and can lower LDL cholesterol by binding bile acids. Colonic bacterial fermentation produces short-chain fatty acids, especially butyrate, which support colonic mucosa. Adequate fluids are needed; sudden high intake may cause bloating."),
('2. Regulation of gastric juice',"See Short Note 10. In summary, ACh, gastrin and histamine stimulate acid secretion; somatostatin, prostaglandins and intestinal feedback inhibit it. Control occurs in cephalic, gastric and intestinal phases."),
('3. Gastrointestinal hormones',"Major hormones: <b>Gastrin</b> from G cells increases acid secretion and mucosal growth. <b>CCK</b> from I cells increases pancreatic enzymes and gallbladder contraction, and slows gastric emptying. <b>Secretin</b> from S cells increases pancreatic/biliary bicarbonate and inhibits gastric acid. <b>GIP</b> from K cells enhances insulin release after oral glucose and inhibits gastric activity. <b>Motilin</b> initiates MMC during fasting. <b>GLP-1</b> from L cells increases insulin, reduces glucagon and slows gastric emptying. <b>Somatostatin</b> broadly inhibits GI secretion."),
('4. Mechanism of HCl secretion',"See Short Note 9. Carbonic anhydrase generates H+ and HCO3-; the apical H+/K+-ATPase secretes H+, Cl- follows into the canaliculus, and HCO3- enters blood, causing alkaline tide."),
('5. Functions of liver',"See Short Note 8. Remember the headings: bile/bilirubin excretion, metabolism, synthesis, detoxification, storage, immunity and hematologic reservoir."),
('6. Regulation of exocrine pancreatic secretion',"Acinar cells secrete enzymes and duct cells secrete bicarbonate-rich fluid. Vagal ACh and CCK stimulate enzyme secretion, especially after fat and amino acids enter duodenum. Acid entering duodenum releases secretin, which stimulates ductal HCO3- and water secretion to neutralize acid. Cephalic and gastric vagal phases contribute modestly; intestinal CCK-secretin control is most important. Enzymes are secreted mainly as zymogens and activated in intestine, protecting the pancreas."),
('7. Liver function tests',"LFTs assess different processes, not one single function. <b>Hepatocellular injury:</b> ALT and AST. <b>Cholestasis:</b> ALP and GGT, with bilirubin. <b>Excretory function:</b> total/direct bilirubin. <b>Synthetic function:</b> albumin and PT/INR (the most useful acute marker because clotting factors have short half-lives). Interpret patterns with clinical context: high ALT/AST suggests hepatocellular injury; high ALP/GGT suggests cholestasis; low albumin or prolonged INR suggests impaired synthesis, but may have nonhepatic causes."),
('8. Absorption of vitamin B12',"Dietary B12 is released from protein by gastric acid and pepsin, first binds salivary haptocorrin, then is released by pancreatic proteases in duodenum and binds intrinsic factor from parietal cells. The IF-B12 complex binds cubilin receptors in terminal ileum and is endocytosed. B12 enters blood bound to transcobalamin II and is stored mainly in liver. Deficiency occurs with pernicious anemia, gastrectomy, pancreatic insufficiency, ileal disease/resection, bacterial overgrowth or poor intake."),
('9. Megaloblastic anemia',"This is macrocytic anemia due to impaired DNA synthesis, usually from vitamin B12 or folate deficiency. Bone marrow shows megaloblastic maturation; peripheral smear shows macro-ovalocytes and hypersegmented neutrophils. B12 deficiency additionally causes neurologic dysfunction and raises methylmalonic acid; both B12 and folate deficiency raise homocysteine. Treat the cause and replace the correct vitamin. Never give folate alone until B12 deficiency has been excluded, because anemia may improve while neurologic injury progresses."),
('10. Functions of bile',"Bile salts emulsify dietary fat and form micelles needed for absorption of lipids and vitamins A, D, E and K. Bile is also the route for excretion of bilirubin, cholesterol, copper, drugs and metabolites. Its bicarbonate-rich component helps neutralize acid in duodenum. Bile salts undergo enterohepatic circulation, conserving the bile-salt pool."),
('11. Peristaltic movements of GIT',"Peristalsis is a propulsive reflex initiated by distension: circular muscle contracts behind the bolus and relaxes ahead of it, moving contents aborally. The myenteric plexus organizes this pattern; parasympathetic activity enhances it and sympathetic activity inhibits it. It operates in esophagus, stomach, small intestine and colon, with local differences in pattern and function.")]
for t,b in brief: story += [H(t),P(b)]

story.append(PageBreak()); story.append(H('IV. What Will Happen and Why',1))
story += [H('Q1. Effect of phototherapy on bilirubin in hemolytic jaundice of a newborn'),P("Phototherapy <b>lowers the serum unconjugated bilirubin concentration</b>. Blue light, near 450 nm, converts unconjugated bilirubin in the skin into water-soluble structural photoisomers, especially lumirubin. These products can be excreted in bile and urine without requiring hepatic glucuronidation. Thus phototherapy bypasses the neonate's relatively immature conjugating capacity and reduces the risk of bilirubin neurotoxicity (kernicterus). In severe hemolysis, bilirubin production may continue rapidly; monitoring and, if thresholds are met, escalation such as IVIG in selected immune hemolysis or exchange transfusion may be required under neonatal protocols.")]

story.append(PageBreak()); story.append(H('V. Clinical Case Question',1))
story += [P('<b>Case summary:</b> A 36-year-old woman has severe epigastric pain, worse at night and between meals, with weight loss, early satiety, bloating, nausea/vomiting, pallor and fatigue.','Box'),H('a) Most likely diagnosis'),P("The pain pattern is suggestive of <b>peptic ulcer disease, particularly duodenal ulcer disease</b>, commonly related to <i>Helicobacter pylori</i>. However, this patient has <b>alarm features</b>: weight loss, early satiety, persistent vomiting and pallor (possible anemia). Therefore one must urgently exclude <b>gastric ulcer with gastric outlet obstruction and gastric malignancy</b>. The appropriate clinical diagnosis is suspected acid-peptic disease with alarm features, requiring prompt upper-GI endoscopy rather than empiric treatment alone."),H('b) Pathophysiology'),P("Peptic ulceration results from imbalance between aggressive factors (gastric acid, pepsin, <i>H. pylori</i>, NSAIDs) and mucosal defenses (mucus-bicarbonate barrier, prostaglandins, epithelial restitution, mucosal blood flow). <i>H. pylori</i> colonizes gastric mucus, produces urease and causes chronic active gastritis. In antral-predominant infection, reduced somatostatin increases gastrin and acid output, predisposing to duodenal ulceration. Acid injury causes mucosal inflammation, necrosis and an ulcer crater. Pain when the stomach is empty and at night is classically associated with duodenal ulcer. Vomiting, early satiety and bloating raise concern for edema/scarring causing gastric outlet obstruction or for a gastric lesion. Pallor may reflect iron-deficiency anemia from chronic occult GI blood loss; reduced intake can also cause weight loss."),H('c) Management'),P("<b>1. Assess and investigate urgently.</b> Check hemodynamic status and signs of bleeding/obstruction. Obtain CBC with indices, ferritin/iron studies, stool occult blood where appropriate, renal/liver profile and pregnancy test when relevant. Perform upper-GI endoscopy promptly because of alarm features; biopsy every gastric ulcer or suspicious lesion to exclude cancer. Test for <i>H. pylori</i> by biopsy, urea breath test or stool antigen. If obstruction or malignancy is suspected, add appropriate imaging and specialist referral.<br/><br/><b>2. Medical treatment.</b> Start a PPI for acid suppression and avoid NSAIDs, smoking and alcohol. If <i>H. pylori</i> is proven, give guideline-based eradication therapy based on local resistance, allergy and prior antibiotic exposure. A current ACG first-choice empirical regimen for many adults is optimized bismuth quadruple therapy for 14 days: PPI twice daily + bismuth + tetracycline + metronidazole. Clarithromycin-containing triple therapy should not be used unless susceptibility is proven. Confirm eradication at least 4 weeks after antibiotics and after withholding PPI for 2 weeks before testing.<br/><br/><b>3. Treat complications/cause.</b> Correct iron deficiency and nutritional depletion. Manage bleeding endoscopically if present. Persistent vomiting or gastric outlet obstruction may require endoscopic balloon dilatation or surgery depending on cause. A nonhealing or malignant ulcer requires biopsy-led oncologic/surgical management."),P('<b>Safety point:</b> This case is not suitable for self-treatment because persistent vomiting, weight loss, early satiety and pallor are red flags.','Box')]

story.append(PageBreak());story.append(H('References and High-Yield Revision',1))
story += [P('<b>Textbook basis:</b> Guyton and Hall Textbook of Medical Physiology, sections on peristalsis, gastric secretion, intestinal motility and GI hormones; Costanzo Physiology, GI physiology chapters; Robbins & Kumar Basic Pathology, bilirubin and jaundice; Lippincott Illustrated Reviews: Biochemistry, vitamin B12 section.'),P('<b>Current clinical update:</b> The 2024 American College of Gastroenterology guidance recommends optimized bismuth quadruple therapy for 14 days as a preferred empiric regimen in treatment-naive adults with <i>H. pylori</i>, and test of cure after therapy. This is a clinical guideline update and local protocols may differ.'),H('One-minute revision list',2),bullets(['Parietal cell: carbonic anhydrase + H+/K+-ATPase -> HCl; HCO3- to blood -> alkaline tide.','ACh + gastrin + histamine stimulate acid; somatostatin and prostaglandins inhibit it.','Segmentation mixes; peristalsis propels; MMC is the fasting housekeeping wave.','CCK: pancreatic enzymes, gallbladder contraction, delayed gastric emptying. Secretin: bicarbonate.','Prehepatic jaundice: unconjugated; obstructive jaundice: conjugated, dark urine, pale stool, pruritus.','B12 needs intrinsic factor and terminal ileum. B12 deficiency can cause neurologic signs.','Alarm dyspepsia features -> endoscopy, not empirical treatment alone.'])]

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