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Pathology Flashcards

1
Q

What is aneurysm?

A

Localized dilation of a vessel

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2
Q

What are the types of aneurysm?

A

Fusiform: around the circumference
Saccular: bulging from the side

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3
Q

What is the Aetiology of aneurysm

A

Artherosclerosis
Hypertension
infection
connective tissue disorder

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4
Q

what are the complications of aneurysm

A

dilation and rupture
thrombosis
thromboembolism

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5
Q

What is the Clinical presentation of aneurysm

A

Male
hypertensive
smoker
50+

acute abdominal pain
shock

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6
Q

What is GORD?

A

Symptomatic passage of gastric contents  lower oesophagus

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7
Q

What are the risk factors for GORD?

A

***Decreased tone of LOS
Impaired musculoskeletal defences
Increased IAP

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8
Q

Pathophysiology of GORD?

A

Clinical low Ph induce inflammation of lower oesophagus leading to fibrosis, blood loss, ulceration

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9
Q

What is barret’s mucosa?

A

*****squamous epithelium replaced by columnar epithileum

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10
Q

Clinical features for GORD?

A

**Heartburn
dyspepsia
Dysphagia

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11
Q

Management of GORD?

A

Reduce predisposing factors

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12
Q

What meds are used to treat GORD?

A

Histamine (ranitidine)
Proton Pump inhibitors (ozemeprazole)
Antiacids (Mylanta

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13
Q

What is gastritis?

A

Acute inflammation of the gastric lining, which is often diffuse

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14
Q

What is the Aetiology for acute gastritis?

A

****Infective agents: Salmonella, E. Coli

Direct damage: alcohol, NSAIDs

Inhibition of mucosal
replacement: chemotherapy, radiotherapy

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15
Q

Clinical features of gastritis?

A

Epigastric discomfort, nausea, anorexia

Erosion of blood vessel can lead to haematemesis

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16
Q

What is chronic gastritis?

A

chronic inflammation of the stomach, associated with lymphocytic infiltration of the mucosa and damage to the epithelium

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17
Q

Aetiology of chronic gastritis

A

**infection H pilori
autoimune gastritis
vitamin B12 deficiency

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18
Q

What is a peptic ulcer?

A

ulceration in any part of the GIT that is exposed to gastric secretions

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19
Q

What are the sites for ulcers?

A

Duodenal ulcers are more common than gastric - 4:1.

Duodenal ulcers: D1,

Gastric ulcers: lesser curvature

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20
Q

What is H. pylori and how does it work?

A

Bacteria that creates gastric ulcers.
H.pylory produces urease
it releases bacterial toxins
then recruits neutrophils and mast cells to produce further injury.

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21
Q

What are other causes of ulcers?

A

Nsaid
Smoking
familial factors

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22
Q

Clinical features for ulcers?

A 
Epigastric pain
Anorexia, 
dyspepsia, 
nausea, 
vomiting
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23
Q

What are complications of ulcers?

A 
pyloric stenosis
Iron deficiency 
anaemia, 
melena, 
haematemesis
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24
Q

Management for ulcers?

A

H.pilory infection: combination amoxicillin

Other ulcers: Histamine

cease smoking

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25
Q

What is celiac disease

A

Genetically-determined, abnormal, hypersensitivity reaction to gluten or its peptide derivative, gliadin

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26
Q

Who has celiac disease?

A

genetics

type 1 diabetes

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27
Q

What is the pathophysiology of celiac disease?

A

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

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28
Q

what are the complications for celiac?

A

Generalised malabsorption:

Ulcerative jejuno-ileitis:

Increased risk of GIT cancers

Skin disorders

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29
Q

Clinical features celiac?

A

Children: Irritability, failure to thrive, abdominal distension
Voluminous, pale stool

Adults: Weight loss, diarrhoea
Abdominal discomfort, excessive flatus
Fatigue
Amenorrhea

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30
Q

Management for celiac

A

Blood test

Endoscopy

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31
Q

What is Jaundice?

A

Yellow appearance of skin, sclerae and mucosa membranes

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32
Q

Why pathologies cause jaundice?

A

liver disease

extra hepatic disorder caused by elevated bilirubin

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33
Q

How does bilirubin metabolism work?

A

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

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34
Q

What are the classification or different types of jaundice?

A
  • Haemolitic jaundice: RBC destruction
  • hepatic jaundice: impaired hepatocyte disfunction (hepatitis, cirrhosis)
  • Neaonatal jaundice: babies
  • Cholestatic jaundice: obstruction of bile ducts
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35
Q

What is viral hepatitis?

A

Infection by hepatitis virus, leading to inflamed liver

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36
Q

what is the pathophysiology of viral hepatitis?

A

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
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37
Q

What types are the 3 types of hepatitis virus ?

A

Hepatitis A
Hepatitis B
Hepatitis C

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38
Q

how does hepatitis A work?

A
  • Transmission: Faecal-oral route
  • Severity: Usually mild, worse in older patients
  • Chronicity: Very rare
  • Vaccination: Yes
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39
Q

how does hepatitis B work?

A
  • Transmission: Parenteral, sexual contact, perinatal
  • Severity: Mild to severe (mortality ~10%)
  • Chronicity: Common
  • Vaccination: Yes
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40
Q

how does hepatitis C work?

A
  • Transmission: Parenteral, perinatal, possibly sexual
  • Severity: Usually mild
  • Chronicity: Very common
  • Vaccination: Not available
41
Q

What are the clinical features in the 4 stages of acute hepatitis?

A

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

42
Q

What are the clinic features of chronic hepatitis?

A

Persistance inflammation 6/12<

complication:
- liver cirrhosis
- liver cancer

43
Q

What is the management for Hepatitis?

A

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
44
Q

What is alcoholic liver disease?

A

When the liver can no longer breakdown alcohol and fails.

potential hyperplasia and hypertrophy

45
Q

Describe the 1st stage of alcoholic liver disease (fatty liver)?

A

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

46
Q

Describe the 2nd stage of alcoholic liver disease (alcoholic hepatitis)?

A

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
47
Q

Describe the 3th stage of alcoholic liver disease (cirrhosis)?

A

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

48
Q

What are other causes of cirrhosis?

A

cholesterol
non-alcoholic liver disease
hepatitis
metabolic disorder

49
Q

What are the manifestations of portal hypertension?

A

Ascites
splenomegaly
varicose veins

50
Q

What are the manifestations of hepatocellular failure?

A

Hepatic encephalopathy
coagulation defects
endocrine changes
peripheral oedema

51
Q

What is the management for alcoholic liver disease?

A

Cease alcohol
improve nutrition
carefully monitor medications
treat complications

prognosis poor

52
Q

Define liver tumour and mention the 3 types tumours?

A

Tumor formation in liver

  • benign tumour
  • primary malignant liver tumour
  • secondary malignant liver tumour
53
Q

What is hepatocellular carcinoma?

A

primary malignant tumour arising from liver epithelial cells (hepatocytes)

54
Q

What are the risk factors for hepatocellular carcinoma?

A

Cirrhosis, viral hepatitis (HBV & HCV)
•Exposure to aflatoxins
•More common in men

55
Q

What are the clinical features for hepatocellular carcinoma?

A

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

56
Q

What are the management for hepatocellular carcinoma?

A

radiofrequencey ablation

partial hepatectomy

57
Q

What are Cholelithiatis?

A 
gallstones formed by 
cholesterol
oestrogen
bile salts 
phopholipids
58
Q

What are the 2 types of gallstones?

A

cholesterol variety

pigment variety

59
Q

What are the clinical features of gallstones?

A

asymptomatic

60
Q

What is the acute cholecytis complication?

A
  • 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
61
Q

List the gallstone complications

A
  • chronic colecystitis
  • mucocele development: filled with fluid
  • infection
  • increased risk of carcinoma
  • choledocholithiasis: stone stuck in bile duct
  • acute pancreatitis: obstruction of hepatopancreatic ampulla
62
Q

What is the management for gallstones?

A

Surgery (cholecystectomy)
oral bile acid therapy
extracorporeal shock wave

63
Q

What is constipation

A

bowel movement less frequent than 3/7

64
Q

Ateiology of constipation?

A 
diet
sedentarism
medications
stress
malignancy
65
Q

Management for constipation?

A

Increase fibre and water
Introduce exercise

modify drugs
address stress

66
Q

What are the different types of laxatives

A

First line:

  • Bulking agents
  • osmotic laxatives

stool softener
bowel stimulant
opioid antagonist

67
Q

What is diarrhoea?

A

Acute
>3 losse stools a day for less than 14 days

Chronic >4/52

68
Q

Common causes of acute diarrhoea ?

A

Food allergy
infectious gastroenteritis
adverse drug reaction

69
Q

Common causes of Chronic diarrhoea ?

A

Chronic infective diarrhoea
Intestinal disorders
Adverse drug reactions (alcohol)

70
Q

Management for diarrhoea

A 
treat cause factor
rehydration + electrolytes
Antibiotics (bacterial)
Anti- diarrhoea agents
opioids: act on GIT opiod receptor
71
Q

What is IBS?

A

Functional bowel disorder consisting of abdominal discomfort and constipation or diarrhoea

72
Q

Mechanism fro IBS?

A

Hyper-excitability of ENS,

caused by food, infection, emotional

73
Q

Clinical features of IBS

A

abdominal Pain Rt/Lt iliac region.
Variable bowel habit
abdominal distention
nausea, cramping, tenesmus

74
Q

Management for IBS?

A

food elimination process

Pharmacology:
Serotonin
Antispachmodic

75
Q

What is diverticular disease?

A

Formation of a pouch in the colon.

76
Q

Pathophysiology of diverticular disease

A

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

77
Q

Complication of diverticular disease

A 
Diverticulitis
Absess formation
fistula
fibrosis
haemorrhage
78
Q

Clinical features diverticular disease

A

Asymptomatic
P lt illicc fossa
change in bowel habit

Acute diverticulitis: severe pain, guarding, rigidity

Abscess formation: palpable mass

79
Q

Management Diverticulosis and diverticulitis

A

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

80
Q

What is Haemorrhoids

A

Internal haemorrhoid: varicosity of the superior rectal vein (proximal to pectinate line)

External haemorrhoid: varicosity affecting the perianal venous plexus (distal to pectinate line)

81
Q

What are the classifications of haemorrhoids

A

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

82
Q

Aetiology of haemorrhoids

A

low fibre diet
chronic cough
obesity
pregnancy

83
Q

complications of haemorrhoids?

A

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

84
Q

Management of haemorrhoids?

A

Ointment: Hydrocortisone/Cinchocaine Ointment

increase fibre

surgery

85
Q

Define appendicitis

A

inflammation of the appendix due to infection

86
Q

Aetiology of appendicitis?

A

obstruction of the lumen and consequent bacterial infection

Obstruction due to stool (faecolith), tumour or foreign body

87
Q

Pathophys of apendicitis

A

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

88
Q

Clinical features for appendicitis

A

abdominal P: gastric + periumbilical region

visceral P RLQ

vomiting nausea anorexia fever diarrhoea or constipation

89
Q

Management for apendicitis

A

Surgery

90
Q

define IBD

A 
chronic inflammatory bowel disease causing ulceration of colonic mucosa in rectum and sigmoid
 due to:
Genetic predisposition
Autoimmune dysfunction 
Abnormal gut microflora
91
Q

Pathophys IBD

A

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

92
Q

Clinical features bowel disease?

A 
diarrhoea
constipation
pain 
tenderness
cramping
tenesmus
93
Q

What is crohns disease?

A

A chronic inflammatory disorder that can affect any part of the GIT from the mouth to the anus

94
Q

Pathophys of crohns disease

A

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

95
Q

Clinical features crohns?

A

Diarrhoea
weight loss
abd p

congintivitis
ankilosis spondilosis
biliary tree disorders 
skin disorder 
kidney stones
96
Q

Complicaitons IBD

A

colorectal cancer
bowel obstruction
toxic megacolon
chronic anal fissures

97
Q

Meds for IBD

A

Anti-inflammatory:

  • Corticosteroids
  • 5-AMinosalicylic acid

Biological agents
immunosupressants
Anti diarrhoeal agent

98
Q

Management IBD

A

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

SBO5 (16 decks)

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