Pathology Flashcards
What is aneurysm?
Localized dilation of a vessel
What are the types of aneurysm?
Fusiform: around the circumference
Saccular: bulging from the side
What is the Aetiology of aneurysm
Artherosclerosis
Hypertension
infection
connective tissue disorder
what are the complications of aneurysm
dilation and rupture
thrombosis
thromboembolism
What is the Clinical presentation of aneurysm
Male
hypertensive
smoker
50+
acute abdominal pain
shock
What is GORD?
Symptomatic passage of gastric contents lower oesophagus
What are the risk factors for GORD?
***Decreased tone of LOS
Impaired musculoskeletal defences
Increased IAP
Pathophysiology of GORD?
Clinical low Ph induce inflammation of lower oesophagus leading to fibrosis, blood loss, ulceration
What is barret’s mucosa?
*****squamous epithelium replaced by columnar epithileum
Clinical features for GORD?
**Heartburn
dyspepsia
Dysphagia
Management of GORD?
Reduce predisposing factors
What meds are used to treat GORD?
Histamine (ranitidine)
Proton Pump inhibitors (ozemeprazole)
Antiacids (Mylanta
What is gastritis?
Acute inflammation of the gastric lining, which is often diffuse
What is the Aetiology for acute gastritis?
****Infective agents: Salmonella, E. Coli
Direct damage: alcohol, NSAIDs
Inhibition of mucosal
replacement: chemotherapy, radiotherapy
Clinical features of gastritis?
Epigastric discomfort, nausea, anorexia
Erosion of blood vessel can lead to haematemesis
What is chronic gastritis?
chronic inflammation of the stomach, associated with lymphocytic infiltration of the mucosa and damage to the epithelium
Aetiology of chronic gastritis
**infection H pilori
autoimune gastritis
vitamin B12 deficiency
What is a peptic ulcer?
ulceration in any part of the GIT that is exposed to gastric secretions
What are the sites for ulcers?
Duodenal ulcers are more common than gastric - 4:1.
Duodenal ulcers: D1,
Gastric ulcers: lesser curvature
What is H. pylori and how does it work?
Bacteria that creates gastric ulcers.
H.pylory produces urease
it releases bacterial toxins
then recruits neutrophils and mast cells to produce further injury.
What are other causes of ulcers?
Nsaid
Smoking
familial factors
Clinical features for ulcers?
Epigastric pain Anorexia, dyspepsia, nausea, vomiting
What are complications of ulcers?
pyloric stenosis Iron deficiency anaemia, melena, haematemesis
Management for ulcers?
H.pilory infection: combination amoxicillin
Other ulcers: Histamine
cease smoking
What is celiac disease
Genetically-determined, abnormal, hypersensitivity reaction to gluten or its peptide derivative, gliadin
Who has celiac disease?
genetics
type 1 diabetes
What is the pathophysiology of celiac disease?
Type 4 (Cell-mediated) Hypersensitivity reaction
Immune cells infiltrate lamina propria
T-lymphocytes release inflammatory cytokines
Plasma cells produce IgA antibodies
Damage to mucosa & atrophy of villi
Impaired intracellular metabolism
Elimination of gluten epithelium returns to normal
what are the complications for celiac?
Generalised malabsorption:
Ulcerative jejuno-ileitis:
Increased risk of GIT cancers
Skin disorders
Clinical features celiac?
Children: Irritability, failure to thrive, abdominal distension
Voluminous, pale stool
Adults: Weight loss, diarrhoea
Abdominal discomfort, excessive flatus
Fatigue
Amenorrhea
Management for celiac
Blood test
Endoscopy
What is Jaundice?
Yellow appearance of skin, sclerae and mucosa membranes
Why pathologies cause jaundice?
liver disease
extra hepatic disorder caused by elevated bilirubin
How does bilirubin metabolism work?
Bilirubin is a pigment made during the normal breakdown of senescent RBCs
•RBC lifespan: 100-120 days
•Engulfed by macrophages in spleen & liver
•Haemoglobin broken into heme + globin
•Globin chains: broken into constituent AAs
•Iron: recycled
•Porphyrin ring: converted to unconjugated bilirubin and released into the bloodstream
-Unconjugated bilirubin is hydrophobic and must travel bound to albumin in the circulation
•In the liver, bilirubin is conjugated with glucuronic acid(enzyme: glucuronyl transferase)
•Conjugated bilirubin is water-soluble & released by hepatocytes as a component of bile
•Undergoes reduction by intestinal bacteria to urobilinogen
•Most urobilinogen: excreted in faeces as stercobilin
•A small proportion of urobilinogen enters the portal circulation and is re-excreted by liver
•Remaining urobilinogen excreted by kidneys as urobilin
What are the classification or different types of jaundice?
- Haemolitic jaundice: RBC destruction
- hepatic jaundice: impaired hepatocyte disfunction (hepatitis, cirrhosis)
- Neaonatal jaundice: babies
- Cholestatic jaundice: obstruction of bile ducts
What is viral hepatitis?
Infection by hepatitis virus, leading to inflamed liver
what is the pathophysiology of viral hepatitis?
Virus induces an acute inflammatory reaction, leading to widespread hepatocyte necrosis
- Usually, liver begins to recover before SSx disappear
- Occasionally, severe destruction of whole lobes results in acute hepatic failure
- Chronic hepatitis with cirrhosis (pictured) is particularly associated with HBV
What types are the 3 types of hepatitis virus ?
Hepatitis A
Hepatitis B
Hepatitis C
how does hepatitis A work?
- Transmission: Faecal-oral route
- Severity: Usually mild, worse in older patients
- Chronicity: Very rare
- Vaccination: Yes
how does hepatitis B work?
- Transmission: Parenteral, sexual contact, perinatal
- Severity: Mild to severe (mortality ~10%)
- Chronicity: Common
- Vaccination: Yes
how does hepatitis C work?
- Transmission: Parenteral, perinatal, possibly sexual
- Severity: Usually mild
- Chronicity: Very common
- Vaccination: Not available
What are the clinical features in the 4 stages of acute hepatitis?
Stage 1: Preclinical •Asymptomatic, but virus actively replicating
•Spread during this phase a concern
Stage 2: Prodromal/Pre-icteric
•Anorexia, nausea, vomiting, malaise, headache
•Mild fever, diarrhoea, upper abdominal discomfort
Stage 3: Icteric•Jaundice develops
•Possibly tender hepatomegaly +/- splenomegaly
•HBV: polyarthralgia affecting small joints, skin rash
Stage 4: Convalescent
•Symptoms subside over a course of several weeks
What are the clinic features of chronic hepatitis?
Persistance inflammation 6/12<
complication:
- liver cirrhosis
- liver cancer
What is the management for Hepatitis?
There is no specific treatment. - aim to reduce spread.
- Hep A: bed rest is advised •Diet: should be low in fats but relatively high in proteins
- Avoid hepatic insults: drugs, esp. alcohol
What is alcoholic liver disease?
When the liver can no longer breakdown alcohol and fails.
potential hyperplasia and hypertrophy
Describe the 1st stage of alcoholic liver disease (fatty liver)?
STAGE 1: FATTY LIVER
•Destruction of rough endoplasmic reticulum in hepatocytes reduces the amount of lipoproteins synthesised & secreted – this causes cells to become swollen with lipids
•Mild to moderate changes are reversible
•Clinical features: +/- hepatomegaly
Describe the 2nd stage of alcoholic liver disease (alcoholic hepatitis)?
STAGE 2: ALCOHOLIC HEPATITIS
•Usually superimposed on fatty liver
•Hepatocyte necrosis induces the infiltration of inflammatory cells
- Clinical features: tender hepatomegaly, fever, jaundice, ascites
- Severe cases: a heavy drinking bout may induce encephalon
Describe the 3th stage of alcoholic liver disease (cirrhosis)?
STAGE 3: CIRRHOSIS
•Irreversible: arises due to chronic inflammation and progressive fibrosis
•Regenerating hepatocytes do not conform to normal cytoarchitecture (nodule formation)
•The structural change obstructs nutrient flow (impaired hepatocyte function)
•Death occurs due to complications (hepatocellular failure, portal hypertension)
linical features:•Jaundice, RUQ pain, hepatomegaly (liver shrinks in advanced stages), foetor hepaticus (late)
•Constitutional symptoms: fever, anorexia, nausea, vomiting, weakness, fatigue, weight lossComplications
•Are related to portal hypertension and hepatocellular failure
What are other causes of cirrhosis?
cholesterol
non-alcoholic liver disease
hepatitis
metabolic disorder
What are the manifestations of portal hypertension?
Ascites
splenomegaly
varicose veins
What are the manifestations of hepatocellular failure?
Hepatic encephalopathy
coagulation defects
endocrine changes
peripheral oedema
What is the management for alcoholic liver disease?
Cease alcohol
improve nutrition
carefully monitor medications
treat complications
prognosis poor
Define liver tumour and mention the 3 types tumours?
Tumor formation in liver
- benign tumour
- primary malignant liver tumour
- secondary malignant liver tumour
What is hepatocellular carcinoma?
primary malignant tumour arising from liver epithelial cells (hepatocytes)
What are the risk factors for hepatocellular carcinoma?
Cirrhosis, viral hepatitis (HBV & HCV)
•Exposure to aflatoxins
•More common in men
What are the clinical features for hepatocellular carcinoma?
rregular hepatomegaly, RUQ pain, jaundice
•Symptoms of cirrhosis e.g. ascites
•Constitutional symptoms e.g. anorexia, weight loss, fever
•Can appear as a single mass or as multiple nodules •50% of cases: metastasis to regional lymph nodes, lungs
What are the management for hepatocellular carcinoma?
radiofrequencey ablation
partial hepatectomy
What are Cholelithiatis?
gallstones formed by cholesterol oestrogen bile salts phopholipids
What are the 2 types of gallstones?
cholesterol variety
pigment variety
What are the clinical features of gallstones?
asymptomatic
What is the acute cholecytis complication?
- Impaction in the cystic duct results in biliary stasis
- Acute inflammation arises from chemical irritation
- Clinical features:
- Sudden onset RUQ pain, +/- Rt shoulder referral•+/- fever or chills
- Murphy’s sign: tenderness on RUQ palp., worse w. inspir
List the gallstone complications
- chronic colecystitis
- mucocele development: filled with fluid
- infection
- increased risk of carcinoma
- choledocholithiasis: stone stuck in bile duct
- acute pancreatitis: obstruction of hepatopancreatic ampulla
What is the management for gallstones?
Surgery (cholecystectomy)
oral bile acid therapy
extracorporeal shock wave
What is constipation
bowel movement less frequent than 3/7
Ateiology of constipation?
diet sedentarism medications stress malignancy
Management for constipation?
Increase fibre and water
Introduce exercise
modify drugs
address stress
What are the different types of laxatives
First line:
- Bulking agents
- osmotic laxatives
stool softener
bowel stimulant
opioid antagonist
What is diarrhoea?
Acute
>3 losse stools a day for less than 14 days
Chronic >4/52
Common causes of acute diarrhoea ?
Food allergy
infectious gastroenteritis
adverse drug reaction
Common causes of Chronic diarrhoea ?
Chronic infective diarrhoea
Intestinal disorders
Adverse drug reactions (alcohol)
Management for diarrhoea
treat cause factor rehydration + electrolytes Antibiotics (bacterial) Anti- diarrhoea agents opioids: act on GIT opiod receptor
What is IBS?
Functional bowel disorder consisting of abdominal discomfort and constipation or diarrhoea
Mechanism fro IBS?
Hyper-excitability of ENS,
caused by food, infection, emotional
Clinical features of IBS
abdominal Pain Rt/Lt iliac region.
Variable bowel habit
abdominal distention
nausea, cramping, tenesmus
Management for IBS?
food elimination process
Pharmacology:
Serotonin
Antispachmodic
What is diverticular disease?
Formation of a pouch in the colon.
Pathophysiology of diverticular disease
Recall the longitudinal muscle layer of the colonic wall
The thickness of this layer is not uniform around its circumference (teniae coli)
Weaker areas of the wall exist where arteries penetrate the circular muscles to nourish the mucosal layer
These areas are the characteristic sites for outpouching
Diverticula are most are often are found in parallel rows (however, a single diverticulum can exist)
Most common site is the sigmoid colon
Complication of diverticular disease
Diverticulitis Absess formation fistula fibrosis haemorrhage
Clinical features diverticular disease
Asymptomatic
P lt illicc fossa
change in bowel habit
Acute diverticulitis: severe pain, guarding, rigidity
Abscess formation: palpable mass
Management Diverticulosis and diverticulitis
Asymptomatic diverticulosis
High-fibre diet & increased H2O to bulk up stool
Acute diverticulitis
Antibiotics, analgesia & anti-inflammatories
I.V. fluids, possibly naso-gastric suction
Usually the inflammation resolves
surgery
What is Haemorrhoids
Internal haemorrhoid: varicosity of the superior rectal vein (proximal to pectinate line)
External haemorrhoid: varicosity affecting the perianal venous plexus (distal to pectinate line)
What are the classifications of haemorrhoids
First degree
Vein is distended and may bleed, but remains internal
Second-degree
Prolapse during defecation, but spontaneously reduce
Third-degree & fourth-degree
Remain protruding after defecation
Aetiology of haemorrhoids
low fibre diet
chronic cough
obesity
pregnancy
complications of haemorrhoids?
Strangulation
Irreducible haemorrhoids compressed by anal sphincter
Patients with acute pain
Thrombosis: acute pain, tender swelling +/- infection, ulceration, gangrene
Healing with fibrosis: can result in skin tags and an increased risk for anal fissures
Persistent blood loss: iron deficiency anaemia
Management of haemorrhoids?
Ointment: Hydrocortisone/Cinchocaine Ointment
increase fibre
surgery
Define appendicitis
inflammation of the appendix due to infection
Aetiology of appendicitis?
obstruction of the lumen and consequent bacterial infection
Obstruction due to stool (faecolith), tumour or foreign body
Pathophys of apendicitis
Obstruction of the lumen prevents proper drainage
As mucosal secretions continue, intraluminal pressure increases (decreases mucosal blood flow)
Hypoxia-induced ulceration promotes bacterial invasion & inflammation
Gangrene develops from thrombosis of the luminal blood vessels, followed by perforation of the appendix
Complications: Peritonitis, abscess formation
Clinical features for appendicitis
abdominal P: gastric + periumbilical region
visceral P RLQ
vomiting nausea anorexia fever diarrhoea or constipation
Management for apendicitis
Surgery
define IBD
chronic inflammatory bowel disease causing ulceration of colonic mucosa in rectum and sigmoid due to: Genetic predisposition Autoimmune dysfunction Abnormal gut microflora
Pathophys IBD
Inflammation begins at the crypts of large intestine, but does not usually spread beyond the submucosa
Most severe at rectum & sigmoid colon (40% of cases spread to the appendix, terminal ileum rarely affected)
Mucosa becomes swollen & hyperaemic (contains excess blood and readily bleeds)
Small erosions form and develop into ulcers (mucosa adopts a ragged appearance)
Healing with fibrosis leads to pseudopolyp formation (clumps of granulation tissue)
Oedema & thickening of the muscularis narrows the lumen
Clinical features bowel disease?
diarrhoea constipation pain tenderness cramping tenesmus
What is crohns disease?
A chronic inflammatory disorder that can affect any part of the GIT from the mouth to the anus
Pathophys of crohns disease
Inflammation begins in the submucosa and spreads to involve the entire thickness of the intestinal wall
Most common sites: terminal ileum, ascending colon & transverse colon
Skip lesions: inflammation can affect some regions of the GIT but not others (rectum is seldom involved)
Chronic inflammation leads to the development of granulomas (clusters of modified macrophages)
These occur in the gut wall, mesentery & mesenteric lymph nodes
The intestinal wall adopts a cobblestone appearance, due to lines of ulceration surrounding areas of mucosal swelling
Clinical features crohns?
Diarrhoea
weight loss
abd p
congintivitis ankilosis spondilosis biliary tree disorders skin disorder kidney stones
Complicaitons IBD
colorectal cancer
bowel obstruction
toxic megacolon
chronic anal fissures
Meds for IBD
Anti-inflammatory:
- Corticosteroids
- 5-AMinosalicylic acid
Biological agents
immunosupressants
Anti diarrhoeal agent
Management IBD
dietary change
Severe Exacerbations:
Hospitalisation required
Rehydration, plasma or blood transfusions
Exclusive enteral nutrition: useful in achieving remission
Sometimes total parenteral nutrition may be necessary
surgery
