Conditions And Clinical Stuff Flashcards by Haris Muhammad

Hernias.

Non-stuck vs stuck hernia symptoms.

Why are femoral hernias more common in women?

Give two differentials.

Which hernias are associated with a low strangulation risk?

Give two complications of gastroschisis.

Lump/ fullness/ swelling with non-stuck

N/V, pain and cannot be moved when stuck

Wider angle of pelvis

Femoral artery anuerysm
Inguinal lymph node swelling

Para-umbilical hernias

intestinal atresia and inflammation

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Xerostomia.

What is oral dysesthesia?

Give three nerves that can be damaged in submandibular gland excision.

Give 3 diseases associated with xerostomia.

Burning sensation in the mouth

Lingual nerve
Hypoglossal nerve
Facial nerve (marginal mandibular branch)

Coeliac disease
Sjrogen syndrome
Sicca syndrome

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Define dyspepsia.

Give some of these upper GI symptoms.

Give two causes of dyspepsia.

Upper GI tract symptoms which are present for four or more weeks

Upper abdominal pain
Heartburn
Acid reflux
N?V

GERD
Gastritis

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GORD.

Give some protective factors of the LOS.

Give some consequences of it.

give 3 pharmacological treatments.

Acute angle of entry
Right crus of the diaphragm
Muscular element
Intra-abdominal segment

Oesophagitis
Strictures
Barrett’s
Ulceration

Antacids
H2 antagonists
PPIs

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Acute gastritis.

How does chemotherapy affect it?

Other than NSAID use and alcohol give another cause.

What is acute erosive haemorrhagic gastritis?

Why does acute gastritis typically affect the greater curvature?

Curlings gastritis?

Reduced epithelial cell proliferation

Bile reflux
Stress (shock)

Severe damage leaving erosions and haemorrhages - dark punctatae amongst hyperaemic mucosa

Due to gravity

Burn patients - decreased plasma volume - shock

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Chronic gastritis.

What are the two broad causes of this and where in the stomach do they typically affect?

Why will gastrin be high in autoimmune?

Give two sequelae of H bacteria pylori.

What risk factors i HBP associated with?

Give three tests that can be done for HBP?

What is Tx?

Autoimmune typically - body
Helicobacter pylori - antrum

Destruction of parietal cells - Reduced negative feedback on gastrin production

Adenocarcinoma
Peptic ulcer

Poverty/rural areas.

Stool antigen
Blood antigen
Urea breath test

Amoxicillin (clarithro + metronidazole)

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Menetrier’s disease.

What is this?

What appearance does the stomach take?

Complication?

Increased TGFa
Gastric hypertrophy

Cerebriform

Pre-cancerous - adenocarcinoma

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PUD.

Why is duodenal PUD associated with weight loss?

Brunner’s gland?

Consequences of PUD.

Because eating decreases the pain

Hypertrophy in duodenal PUD

Malignancy rarely
Haemorrhage
Perforation
Erosion intro adjacent structure

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Coeliac disease.

Give 3 markers in the blood.

Give three things seen on histology.

Why may a rash occur?

What cancers are the predisposed to?

Give two reasons why osteoporosis may occur?

Genetic factors?

IgA to endomysium tTG and lamina propia tTG
IgA to gliadin

Villious atrophy
Intestinal crypt hyperplasia (lengthening)
Lymphocyte infiltrating epithelium

Eczema herpetiformis - IgA binding to tTG in skin

Small intestinal cancer
T cell lymphoma

Impaired calcium absorption
Vitamin D deficiency
Dystrophic calcification of fatty acids

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Collagen.

What can lysyl oxidase deficiency be caused by?

What can prolylhydroxylase defiency be caused by?

Defiency of B6 and Cu2+

Vitamin C and Fe2+

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Cirrhosis.

Give some extra-hepatic manifestations of cirrhosis.

Give two signs that can be indicative of ascites.

Give some complications of cirrhosis.

Give two ways in which stellate cells lead to portal hypertension.

Parotid gland swelling (alcohol related) 
Asterixis 
Testicular atorphy 
Palmar erythema
Dupeytrens contracture

Puddle sign
Shifting dullness

Portal hypertension
Ascites
Hepatorenal syndrome
Hepatic encephalopathy

Deposit fibrous tissue
Constriction of sinusoids

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Haemochromatosis.

Give some ways iron is lost from the body.

Give some places iron can be deposited.

Why may it present later in women?

Give some extra-hepatic manifestations of it.

Two treatments/

Desquamation of skin
Sweat
GI tract

Liver, heart, pancreas, skin, joints and pituitary

Because they can also lose iron through menstrual bleeding.

Type I DM/ malabsorption 
Bronze pigment 
Amenorrhea/ testicular atrophy 
Cardiomyopathy leading to arrythmias 
Degenerative joint disease

Therapeutic phlebotomy
Deferroxamine

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Wilson’s disease.

Defect in?

When do symptoms typically present?

Blood tests?

Why anaemia?

Treatments.

Autosomal dominant defect in ATP7B

Late childhood.

Low caeruloplasmin
Increased Cu in blood (and urine)

Circulating Cu causes damaged to RBCs.

Penicillamine (copper chelation)
Zinc + amminoum tetrathiomolybdate
Liver transplant

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Primary sclerosising cholangitis.

What is affected?

What does the fibrosis look like on ERCP and on histology?

Associated with?

Why decreased urobilinogen in PSC?

Men or women?

ABs?

Fibrosing of intra and extra hepatic bile ducts

Onion skin fibrosis
Beaded bile duct appearance

UC and Crohn’s

Bile flow obstruction means that bilirubin can not get into the gut to be converted to urobilinogen by gut bacteria and therefore no urobilinogen can be absorbed and subsequently exerted into urine by the kidney;.;

Men

ANCA

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Primary billiary cirrhosis.

Pathophysiology?

M or F?

Associated with?

Markers?

Why might xanthomas form?

How distinguish from secondary biliary cholangitis/ cirrhosis?

T cells attach the intrahepatic bile ducts leading to their destruction

Female

Sjrogen and AI hepatitis
RA

AMAa

Cholesterol from bile backlogging and leading to deposition under skin

No AMAs in the blood

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Varices.

Where do they occur?

What is the portal and systemic circulation involved with paraumbilical ones?

Oesophageal?

Rectal?

Portosystemic anastomoses

Paraumbilical veins (ligamentum teres) and superficial epigastric vein

Esophageal branches of the left gastric vein and eosophageal branches of azygous vein.

Superior rectal vein with middle and inferior rectal veins.

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Hepatorenal syndrome.

Why kidney damage?

Why ascites?

Because vasodilator release resulting in hypotension and reduced renal perfusion

Also RAAS activation will causes renal artery vasoconstriction and further reduce blood flow to the kidney.

Because RAAS activation leading to increased Na and H2O retention

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Cholelithiaisis.

Name a radiolucent and radio opaque type.

Why does COCP predispose?

What are brown gall stones often caused by?

Radio lucent - cholesterol stones
Radio opaque - bilirubin stones

Increased cholesterol due to estrogen adverse effects on the lipid profile.

Gall bladder infection or biliary tract infection

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Acute cholecystitis.

Pain where?

Other symptoms?

Sign?

Why may gallbladder become ischaemic?

Epigastric that localises to the RUQ

N/V Fever

Murphy’s sign

Increased pressure in the cystic duct overtime leads to compression of blood vessels

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Ascending cholangitis

Associated with usually?

Charcots triad and Reynolds Pentad?

Choledocolithiasis

Charcots triad - jaundice, fever RUQ pain
Reynolds pentad - confusion and hypotension

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Acute Pancreatitis.

Two main causes?

Why does alcohol cause it?

Why may they have a palpable mass?

Give some complications.

Two signs.

Alcohol abuse
Gall stones

Increased zymogen secretion but reduced fluid and bicarbonate secretion from ductal cells - block duct with viscous plug.
Also stimulate cytokines

Pancreatic pseudocyst

Haemorrhage (shock)
DIC
ARDS (vasodilation throughout body makes it hard to breathe)

Cullens
Grey turners sign

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Chornic pancreatitis.

What is the main cause in children?

Complications.

Cystic fibrosis

Weight loss
DM Type 1
Pseudocysts
Pancreatic cancer

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LFTs,

Which one is more acute?

More specific to liver?

Which one rises in alcoholic hepatitis?

ALT

AST

UC.

How can it involved the ileum?

3 skin manifestations.

Give some pathological changes.

Barium enema finding?

Why granular appearance?

Backwash ileitis caused by an incompetent ileocaecal valve

Erythema nodusum
Pyoderma gangrenosum
Psoriasis

Crypt distortion
Reduced goblet cell number
Crypt abscess

Lead pipe colon

Contrast settling in the superficial ulcers

Diarrhoea. Give one cause of osmotic and secretory diarrhoea.

Lactose intolerance | Congenital chloridorrhea/ bacterial infections

Constipation. Two dietary factors. Most common cause? Give three causes of primary constipation.

Decreased fibre, decreased fluids High milk, coffee, tea and alcohol Lifestyle factors. Normal transit Slow Transit Pelvic floor dysfunction

Appendicitis. Give two things that may lead to obstruction of the lumen. 2 complications. In what two positions of the appendix might you not got typical RIL pain? What two differentials might you consider?

Faecalith Lymphoid hyperplasia Foreign body Abscess (periappendiceal and subphrenic) Perforation Retrocaecal Pelvic Ectopic pregnancy UTI

Diverticulosis. Cause? Why does it most likely occur in the sigmoid colon? Give one other dietary cause and 2 genetic.

High pressure due to low fibre diet Smallest lumen and therefore according to laplaces law will have the highest pressure. Marfans genetic EDS geneti High red meat and fatty foods - dietary

Diverticulitis. Why is rectal bleeding more associated with diverticulosis? Common fistula? Common presentation?

Because the blood vessels become scarring due to inflammation in diverticulitis Colovesicular fistula LLQ pain + haematochezia + fever + bloating +/- peritonitis signs Reduced bowel sounds.

What is relevance of the anorectal ring? Which sphincter forms more of the resting pressure of the anal sphincter? Give three responses in the defecation reflex once food reaches the rectum.

Fusion of the IAS and EAS Palpable on DRE IAS (circular muscle thickening -80%) Contraction of rectum IAS relaxes EAS contracts

Haemorrhoids. Give some risk factors. Give cause of anal fissure. Where do they usually occur?

Pregnancy Straining Low fibre Heavy weight lifting Increased internal anal sphincter tone Posterior midline.

Peritonitis. Difference between primary and secondary. Give another cause of secondary other than perforation.

Primary is when there is no acute abdominal disease and instead haematogenous/ lymphatic spread of the bacteria occurs usually when there is an underlying disease causing ascites (cirrhosis) Secondary - acute abdominal condition - perforation occurs. Tubal pregnancy/ ovarian cyst

Bowel obstruction. 2 common causes in children and adults. Intussusception Common location of intussusception. Give two possible lead points. Triad? Sign?

Children - intussusception and intestinal atresia Adults - adhesions and incarcerated hernias Ileocaecal region due to lax mesentery of sigmoid colon Meckel’s diverticulum and enlarged lymph node Haematochezia, abdominal pain and vomiting Dance sign - right hypochondrium mass with RLQ emptiness.

Small bowel obstruction. Early symptoms? Give 2 causes. Abdo pain pattern vs large?

Nausea and billious vomiting Adhesions - post-op Infection - post-op - exudation of fibrous tissue damaging the mesothelium Crohn’s Hernia Colicky - 3-4 mins whereas in large bowel every 10-15 minutes.

Large bowel obstruction. Common causes? Early symptoms? Why can higher fibre diet predispose to volvulus? Why can one bout of volvulus predispose to further?

Colon cancer Diverticula disease Volvulus Change in bowel habit - constipation. Overloading of the sigmoid colon leading to elongation compared to its mesenteric attachment acting as a pivot for twisting. Mesocolon becomes further shortened due to chronic inflammation and adhesions forming at the base of it.

Acute mesenteric Ischaemia. Common in? Typical presentation? When will metabolic acidosis occur? Give some other complications. Gold standard investigation?

Females with PVD (Left sided) severe abdo pain disproportionate to clinical examination due to very little tenderness Comes on 30 minutes after eating and will last 4 hours. +/- N/V When bowel has become necrotic MODS Sepsis and septic shock Bowel necrosis Death CT angiography.

Oesophageal varices. Treatment?

Band ligation TIPS Terlipressin

AAA. Classify? Why nausea and back pain? What is the cause of aneurysm in syphillis? Why might X-ray be useful for looking at aneurysms? Surgical Tx?

Dilatation 1.5 times the size. Compress stomach and vertebrae. Endarteritis obliterans See if calcification has occured. Endograft

Faecal microbiota transplant. USes?

PC C diff infection IBD symptoms

Salmonella gastroenteritis. Incubation period? Resolves within? How do they causes lymphoid hyperplasia?

Around 48 hours. 2-3 days. Endocytosed into small intestine cels then movie out basolateral side where they are taken up by macrophages which take them to the reticuloendothelial system where they multiply. They can then re-enter the bowel via the gall bladder and liver.

Campylobacter jejunum. Gram stain. Incubation period? Spread?

gram negative rods with S/ C/ spiral shaped appearance 1-7 days Resolution - days to weeks Faecal oral route

Shigella. Why does it cause bloody diarrhoea? Why is crowding a risk factor? What is S dysenteriae asscoaited with? What can be said about the stools? Mainly affects? Resolution?

Because it enters enterocytes via endocytosis and then multiplies inside and forms abscesses as the cells die and as they die it spreads to adjacent cells. Low infectious dose (10-100) viable organisms needed. Shiga toxin - HUS and haemorrhagic colitis Bloody + mucus Elderly, young and malnourished Within a week

E.coli. What are the following most commonly associated with? ``` ETEC EPEC EHEC EIEC EAEC ``` Why not antibiotics in EHEC?

Travellers diarrhoea Watery diarrhoea in infants with poor sanitation in developing countries Haemorrhagic colitis and HUS Bloody diarrhoea Persistent diarrhoea in young children and HIV infected. Can potentiate HUS.

C diff. Give 4 ABx that predispose? Two complications?

Clindamycin Amoxicillin Cephalosporins Ampicillin CACA PMC TMC

Noro virus. Character of the fever? Why diarrhoea?

Low grade Brush border enzyme disruption. Anion secretion into the gut lumen.

Cryptosporidium. Spread? Why diarrhoea? Extreme systems in? Name another chlorine resistant microbe.

Bodies of water Faecal oral Chloride secretion Brush border enzyme disruption AIDs patients Giardia

Giardiasis causative organism? Giardia lamblia Incubation? Complication? History can be typical of?

LONG INCUBATION - 10+ days after the posture Lactose intolerance Camping and hiking and drinking mountain water.

Entamoeba histolytica. RFs? How can you detect this and Giardia? Where does excystation occur ? Complication?

Travelled to developing places which are topical with poor sanitation. MSM Cysts in the faeces? Colon both occur in the colon (giardia aswell) Liver abscess

Oesophageal cancer. Main people affected? Give four risk factors. Most common appearance? 5 red flags with dysphagia.

50-60s Afro Caribbean males Achalasia Barrett’s Smoking Chronic alcohol Ulcerating ``` Anorexia Loss of weight Anaemia Recent onset of progressive symptoms Masses/Malaena ```

Gastric cancer. Main type of tumour? Give two stromal tumours that occur? What is the term linitis plastica used to refer to? Risk factors.

Adenocarcinoma. GISTs (interstitial cells of canal tumours) and leiomyomas Diffusers infiltrating Gastric adenocarcinoma leaving a thickened wall with a leathery inelastic consistency. ``` High salt diet Smoking H pylori FHx Chronic inflammation occurring. ```

Carcinoid tumours Why flushing? Why asthma, shortness of breath and wheezing? Why heart valve lesions and endocardial fibrosis? Why pellagra? Why octreoscan? Urinalysis?

Histamine and bradykinin release leading to vasodilation and flushing Serotonin leading to bronchoconstriction Serotonin causes fibrosis in the heart Serotonin - tryptophan used up - needed for B3 synthesis and therefore pellagra. Octreotide binds to somatostatin receptors which are highly expressed by carcinoid tumours. 5-hydroxyindoeacetic acid is serotonin metabolite

Cholangiocarcinomas. Give two associations. Give red flags of jaundice.

PSC Parasitic liver disease Craggy border hepatomegaly Unintentional weight loss Ascites Painless

Pancreatic cancer. Risk factors. Gene associated? Two clinical signs associated? Why is radiating pain a bad sign?

``` FHx Smoking Men - more affected than women Increasing incidence with age Chronic pancreatitis Diet high in red meat ``` BRCA2 Trousseau sign of malignancy Courvoisier sign Indicates invasion of the retroperitoneal splanchnic nerve plexus

Large bowel cancer. Why is it important to have well controlled IBD? Give two lifestyle related risk factors. Describe how screening works.

because it reduces cancer risk back to that of the normal population. High fat diet Sedentary lifestyle

Rota virus. Affects typically? Spread?

Typically children (U5s) Faecal oral route