Conditions And Clinical Stuff Flashcards
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
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
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
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
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
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)
Menetrier’s disease.
What is this?
What appearance does the stomach take?
Complication?
Increased TGFa
Gastric hypertrophy
Cerebriform
Pre-cancerous - adenocarcinoma
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
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
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+
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
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
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
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
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
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.
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
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
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
Ascending cholangitis
Associated with usually?
Charcots triad and Reynolds Pentad?
Choledocolithiasis
Charcots triad - jaundice, fever RUQ pain
Reynolds pentad - confusion and hypotension
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
Chornic pancreatitis.
What is the main cause in children?
Complications.
Cystic fibrosis
Weight loss
DM Type 1
Pseudocysts
Pancreatic cancer
