Pathology Flashcards
(98 cards)
1
Q
What is aneurysm?
A
Localized dilation of a vessel
2
Q
What are the types of aneurysm?
A
Fusiform: around the circumference
Saccular: bulging from the side
3
Q
What is the Aetiology of aneurysm
A
Artherosclerosis
Hypertension
infection
connective tissue disorder
4
Q
what are the complications of aneurysm
A
dilation and rupture
thrombosis
thromboembolism
5
Q
What is the Clinical presentation of aneurysm
A
Male
hypertensive
smoker
50+
acute abdominal pain
shock
6
Q
What is GORD?
A
Symptomatic passage of gastric contents lower oesophagus
7
Q
What are the risk factors for GORD?
A
***Decreased tone of LOS
Impaired musculoskeletal defences
Increased IAP
8
Q
Pathophysiology of GORD?
A
Clinical low Ph induce inflammation of lower oesophagus leading to fibrosis, blood loss, ulceration
9
Q
What is barret’s mucosa?
A
*****squamous epithelium replaced by columnar epithileum
10
Q
Clinical features for GORD?
A
**Heartburn
dyspepsia
Dysphagia
11
Q
Management of GORD?
A
Reduce predisposing factors
12
Q
What meds are used to treat GORD?
A
Histamine (ranitidine)
Proton Pump inhibitors (ozemeprazole)
Antiacids (Mylanta
13
Q
What is gastritis?
A
Acute inflammation of the gastric lining, which is often diffuse
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
15
Q
Clinical features of gastritis?
A
Epigastric discomfort, nausea, anorexia
Erosion of blood vessel can lead to haematemesis
16
Q
What is chronic gastritis?
A
chronic inflammation of the stomach, associated with lymphocytic infiltration of the mucosa and damage to the epithelium
17
Q
Aetiology of chronic gastritis
A
**infection H pilori
autoimune gastritis
vitamin B12 deficiency
18
Q
What is a peptic ulcer?
A
ulceration in any part of the GIT that is exposed to gastric secretions
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
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.
21
Q
What are other causes of ulcers?
A
Nsaid
Smoking
familial factors
22
Q
Clinical features for ulcers?
A
Epigastric pain Anorexia, dyspepsia, nausea, vomiting
23
Q
What are complications of ulcers?
A
pyloric stenosis Iron deficiency anaemia, melena, haematemesis
24
Q
Management for ulcers?
A
H.pilory infection: combination amoxicillin
Other ulcers: Histamine
cease smoking
25
What is celiac disease
Genetically-determined, abnormal, hypersensitivity reaction to gluten or its peptide derivative, gliadin
26
Who has celiac disease?
genetics
| type 1 diabetes
27
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
28
what are the complications for celiac?
Generalised malabsorption:
Ulcerative jejuno-ileitis:
Increased risk of GIT cancers
Skin disorders
29
Clinical features celiac?
Children: Irritability, failure to thrive, abdominal distension
Voluminous, pale stool
Adults: Weight loss, diarrhoea
Abdominal discomfort, excessive flatus
Fatigue
Amenorrhea
30
Management for celiac
Blood test
| Endoscopy
31
What is Jaundice?
Yellow appearance of skin, sclerae and mucosa membranes
32
Why pathologies cause jaundice?
liver disease
extra hepatic disorder caused by elevated bilirubin
33
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
34
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
35
What is viral hepatitis?
Infection by hepatitis virus, leading to inflamed liver
36
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
37
What types are the 3 types of hepatitis virus ?
Hepatitis A
Hepatitis B
Hepatitis C
38
how does hepatitis A work?
* Transmission: Faecal-oral route
* Severity: Usually mild, worse in older patients
* Chronicity: Very rare
* Vaccination: Yes
39
how does hepatitis B work?
* Transmission: Parenteral, sexual contact, perinatal
* Severity: Mild to severe (mortality ~10%)
* Chronicity: Common
* Vaccination: Yes
40
how does hepatitis C work?
* Transmission: Parenteral, perinatal, possibly sexual
* Severity: Usually mild
* Chronicity: Very common
* Vaccination: Not available
41
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
42
What are the clinic features of chronic hepatitis?
Persistance inflammation 6/12<
complication:
- liver cirrhosis
- liver cancer
43
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
44
What is alcoholic liver disease?
When the liver can no longer breakdown alcohol and fails.
| potential hyperplasia and hypertrophy
45
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
46
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
47
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
48
What are other causes of cirrhosis?
cholesterol
non-alcoholic liver disease
hepatitis
metabolic disorder
49
What are the manifestations of portal hypertension?
Ascites
splenomegaly
varicose veins
50
What are the manifestations of hepatocellular failure?
Hepatic encephalopathy
coagulation defects
endocrine changes
peripheral oedema
51
What is the management for alcoholic liver disease?
Cease alcohol
improve nutrition
carefully monitor medications
treat complications
prognosis poor
52
Define liver tumour and mention the 3 types tumours?
Tumor formation in liver
- benign tumour
- primary malignant liver tumour
- secondary malignant liver tumour
53
What is hepatocellular carcinoma?
primary malignant tumour arising from liver epithelial cells (hepatocytes)
54
What are the risk factors for hepatocellular carcinoma?
Cirrhosis, viral hepatitis (HBV & HCV)
•Exposure to aflatoxins
•More common in men
55
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
56
What are the management for hepatocellular carcinoma?
radiofrequencey ablation
| partial hepatectomy
57
What are Cholelithiatis?
```
gallstones formed by
cholesterol
oestrogen
bile salts
phopholipids
```
58
What are the 2 types of gallstones?
cholesterol variety
| pigment variety
59
What are the clinical features of gallstones?
asymptomatic
60
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
61
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
62
What is the management for gallstones?
Surgery (cholecystectomy)
oral bile acid therapy
extracorporeal shock wave
63
What is constipation
bowel movement less frequent than 3/7
64
Ateiology of constipation?
```
diet
sedentarism
medications
stress
malignancy
```
65
Management for constipation?
Increase fibre and water
Introduce exercise
modify drugs
address stress
66
What are the different types of laxatives
First line:
- Bulking agents
- osmotic laxatives
stool softener
bowel stimulant
opioid antagonist
67
What is diarrhoea?
Acute
>3 losse stools a day for less than 14 days
Chronic >4/52
68
Common causes of acute diarrhoea ?
Food allergy
infectious gastroenteritis
adverse drug reaction
69
Common causes of Chronic diarrhoea ?
Chronic infective diarrhoea
Intestinal disorders
Adverse drug reactions (alcohol)
70
Management for diarrhoea
```
treat cause factor
rehydration + electrolytes
Antibiotics (bacterial)
Anti- diarrhoea agents
opioids: act on GIT opiod receptor
```
71
What is IBS?
Functional bowel disorder consisting of abdominal discomfort and constipation or diarrhoea
72
Mechanism fro IBS?
Hyper-excitability of ENS,
| caused by food, infection, emotional
73
Clinical features of IBS
abdominal Pain Rt/Lt iliac region.
Variable bowel habit
abdominal distention
nausea, cramping, tenesmus
74
Management for IBS?
food elimination process
Pharmacology:
Serotonin
Antispachmodic
75
What is diverticular disease?
Formation of a pouch in the colon.
76
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
77
Complication of diverticular disease
```
Diverticulitis
Absess formation
fistula
fibrosis
haemorrhage
```
78
Clinical features diverticular disease
Asymptomatic
P lt illicc fossa
change in bowel habit
Acute diverticulitis: severe pain, guarding, rigidity
Abscess formation: palpable mass
79
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
80
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)
81
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
82
Aetiology of haemorrhoids
low fibre diet
chronic cough
obesity
pregnancy
83
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
84
Management of haemorrhoids?
Ointment: Hydrocortisone/Cinchocaine Ointment
increase fibre
surgery
85
Define appendicitis
inflammation of the appendix due to infection
86
Aetiology of appendicitis?
obstruction of the lumen and consequent bacterial infection
| Obstruction due to stool (faecolith), tumour or foreign body
87
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
88
Clinical features for appendicitis
abdominal P: gastric + periumbilical region
visceral P RLQ
vomiting nausea anorexia fever diarrhoea or constipation
89
Management for apendicitis
Surgery
90
define IBD
```
chronic inflammatory bowel disease causing ulceration of colonic mucosa in rectum and sigmoid
due to:
Genetic predisposition
Autoimmune dysfunction
Abnormal gut microflora
```
91
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
92
Clinical features bowel disease?
```
diarrhoea
constipation
pain
tenderness
cramping
tenesmus
```
93
What is crohns disease?
A chronic inflammatory disorder that can affect any part of the GIT from the mouth to the anus
94
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
95
Clinical features crohns?
Diarrhoea
weight loss
abd p
```
congintivitis
ankilosis spondilosis
biliary tree disorders
skin disorder
kidney stones
```
96
Complicaitons IBD
colorectal cancer
bowel obstruction
toxic megacolon
chronic anal fissures
97
Meds for IBD
Anti-inflammatory:
- Corticosteroids
- 5-AMinosalicylic acid
Biological agents
immunosupressants
Anti diarrhoeal agent
98
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
