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Pathology > Clinical Conditions > Flashcards

Clinical Conditions Flashcards

1
Q

What would you see histologically in the liver of a patient who has excessive alcohol intake

A

Mallory hyaline which clumps of cytokeratin

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2
Q

What can excessive alcohol intake cause

A

Fatty liver, cirrhosis, death of hepatocytes, regeneration of liver cells increasing the chance of hepatocellular cancer

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3
Q

How does hepatitis B present

A

Jaundice, flu, nausea, hepatomegaly, splenomegaly

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4
Q

What tests are used to diagnose hepatitis B

A

HBsAg, AST,ALT, albumin, LDH

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5
Q

What is the laboratory diagnosis for acute pancreatitis

A

You will be able to see fat necrosis as the lipases break down fatty acids which then react with calcium to form soap

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6
Q

What is hereditary haemochromatosis

A

When there is too much iron resulting from a mutation in the HFE gene so hepcidin is inhibited

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7
Q

How does hereditary haemochromatosis present

A

Fatigue, pain and cirrhosis

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8
Q

What is alpha-1 antitrypsin deficiency

A

An enzyme deficiency meaning that trypsin cant be broken down

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9
Q

What are the complications of an alpha 1 antitrypsin deficiency

A
  • emphysema as trypsin breaks down the elastase in the lungs
  • liver disease due to a build up of poorly formed proteins
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10
Q

What is coal-workers pneumoconiosis

A

Where the coal dust causes pigmented lungs as the pigment is digested by macrophages in the alveoli - they can then spread to the lymph nodes

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11
Q

What are the complications of pneumoconiosis

A

Inflammation and fibrosis

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12
Q

What are the pathological stages of lobar pneumonia

A
  1. Congestion - an exudate develops in the alveoli
  2. Red hepatisation - lots of RBCs congest
  3. Grey hepatisation - RBCs disintegrate
  4. Resolution
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13
Q

Compare bronchopneumonia and lobar pneumonia

A

In lobar only 1 lobe is affected and you can see a clear separation of where is affected and not
In bronchopneumonia the infection is spread over all the lungs

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14
Q

What are the complications of lobar pneumonia

A

Empyema, lung abscess, sepsis

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15
Q

What is the comments causative organism of lobar pneumonia

A

Streptococcus pneumoniae

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16
Q

What is the appearance of acute appendicitis

A

Red, large, pus (making it look green as its a fibrous exudate)

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17
Q

What are the possible causes of acute appendicitis

A

Infection, perforated bowel, blocked by mucus

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18
Q

What are the complications of acute appendicitis

A

Rupture, perforation, sepsis

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19
Q

What is the appearance of bacterial meningitis

A

Green pus, increase in cerebral pressure causes there to be no ridges and a midline shift

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20
Q

What are the common causative organisms of bacterial meningitis

A

Neonate: E.coli, Group B streptococcus
Children: Haemophilius influenzae, strep pneumoniae, Neisseria Meningitidus
Adults: Neisseria Meningitidus, strep penuamoniae

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21
Q

What are the complications of bacterial meningitidus

A

Seizures, loss of balance, loss of vision, loss of hearing and memory

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22
Q

What are the complications of Gallstones

A

Blockage leads to inflammation can also cause hepatic abscesses when they go into the liver

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23
Q

What liver function test will be high in gallstones

A

ALP as the bile duct may be blocked

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24
Q

How do gallstones cause ascending cholangitis

A

The gallstones block the bile duct giving repeated/chronic inflammation

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25
Q

What is a common causative organism of ascending cholangitis

A

C.diff

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26
Q

What are complications of ascending cholangitis

A

Shock, death

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27
Q

What is hereditary angiotensin-oedema

A

Deficiency of the enzyme C1 esterase inhibitor

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28
Q

How does hereditary angiotensin-oedema present

A

Repeated non-itchy oedema which can cause death if it occurs in the larynx
Gives abdominal pain if occurring in the intestines

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29
Q

What is chronic granulomatous disease

A

When macrophages can produce a respiratory burst as they can’t produce superoxide - gives lots of granulomas

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30
Q

How does Rheumatoid arthritis present

A

Inflammation of the joint with cartilage erosion and rheumatoid nodules which are collections of granulomas.

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31
Q

When is the pain worse in rheumatoid arthritis

A

Worse in the mornings but the pain is symmetrical

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32
Q

Describe the features of ulcerative colitis

A
  • superficial (only affects mucosa and submucosa)
  • only colon affected so increased risk of colon cancer
  • crypts of lieberkuhn abscesses
  • erythema nodosum
  • can also get lower limb ulcers, eye disease and liver disease
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33
Q

Describe the features of Crohn’s disease

A
  • transmural (affects deeper layers of the gut)
  • affects all of the GI tract
  • cobblestone appearance
  • granulomas
  • erythema nodosum
  • strictures
  • fistulae
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34
Q

What are strictures

A

Fibrous narrowing

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35
Q

What are fistulae

A

Connections between mucus lined organs

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36
Q

What is the appearance of the bile duct in chronic cholecystitis

A

Inflammation makes it very fibrous and so transparent

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37
Q

How does H.pylori damage the stomach

A

They release cytokines which damage epithelia and cause inflammation

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38
Q

What are the complications of H.pylori

A

Ulcer, gastric adenocarcinoma, lymphoma (malignancy of lymph tissue)

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39
Q

What is an ulcer

A

A breach in the mucosa

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40
Q

What is cirrhosis

A

Liver damage through scarring giving loss of function

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41
Q

What is the appearance of cirrhosis

A

Macroscopically - Regenerating nodules

microscopically - red areas of regenerating cells and blue fibrosus bands

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42
Q

What are the complications of cirrhosis

A

Scar tissue blocks portal flow giving portal hypertension

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43
Q

What is the pathophysiology of TB

A

Engulfed by macrophages in the lungs but they cant digest the bacteria so cause chronic inflammation and granulomas form

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44
Q

What is the microscopic appearance of TB

A

Langerhan giant cells, caseating granulomas

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45
Q

What is an acid fast test

A

Where you stain the TB sample with acid to retain the stain

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46
Q

What is sarcoidosis

A

Non-caseating Granuloma forming disease of unknown cause

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47
Q

What are the symptoms of sarcoidosis

A

Cough, shortness of breath, coughing up sputum

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48
Q

What is the cause of scurvy

A

Vitamin C deficiency which is needed for proline hydroxylase in collagen production

49
Q

How does scurvy present

A

Poor bone formation, poor wound healing, teeth fall out, old scars reopen

50
Q

What is Ehlers Danlos syndrome

A

Collagen mutation disease

51
Q

What are the symptoms of Ehers-Danlos

A

Stretchy skin, dislocation, bruising, aortic dissection

52
Q

What is osteogenesis imperfecta

A

Type 1 collagen mutation

53
Q

How does osteogenesis imperfecta present

A

Repeated bone breaking/fractures and blue sclera

54
Q

What is Alpert syndrome

A

Collage IV defect

55
Q

How does Alport syndrome present

A

Kidney disease, hearing loss, loss of vision (where collagen IV is present)

56
Q

How does a keloid scar present

A

Raised, red, hairless and shiny

If you cut it away it will just grow back

57
Q

What is a keloid scar

A

Overgrowth of a scar during wound healing.

58
Q

what is Haemophilia A

A

a factor VIII deficiency disease causing poor blood clotting

59
Q

what is the inheritance pattern of haemophilia A

A

x linked recessive

60
Q

what are the signs of haemophilia A

A

bleeding into joints, bleeding excessively (e.g. after dental extractions)

61
Q

what would be the laboratory abnormalities of haemophilia A

A

low factor VIII, increase in APTT, normal PT and bleeding time

62
Q

what is haemophilia B

A

deficiency in Factor IX

63
Q

what is Von Willebrand disease

A

a vWF deficiency

64
Q

what is the inheritance pattern of Von Willebrands disease

A

autosomal dominant

65
Q

what does Von Willebrands factor do

A

allows for platelets to bind to cause blood clotting and also stabilises factor VIII

66
Q

what are the laboratory abnormalities in Von Willebrands disease

A

low factor VIII, increase APTT, increase D-dimers, normal PT, increased bleeding time

67
Q

what is the presentation in von willebrands disease

A

poor blood clotting as platelets cant attach to injured vessels and aggregate also low factor VIII

68
Q

what is immune thrombocytopenic purpura

A

autoimmune disease against the surface antigen on platelets

69
Q

how does immune thrombocytopenic purpura present

A

purpuric rash and bleeding

70
Q

what are the laboratory abnormalities in immune thrombocytopenic purpura

A

low platelet, increased bleeding time, normal PT and APTT

71
Q

true or false: the treatment for immune thrombocytopenic purpura is platelet treatment

A

false - as these new platelets will also be rejected

72
Q

gives examples of types of thrombophilias

A

Protein C deficiency, factor V Leiden

73
Q

what happens with a thrombophilia disease

A

you have an increase in clotting

74
Q

how do thrombophilia diseases present

A

as a DVT - pain, red, warm, swelling

75
Q

what can cause DIC

A

trauma, sepsis, burns, snake bite and fractures etc

76
Q

what is DIC

A

disseminated intravascular coagulation is when you have lots of microthrombi form due to an increase in thrombin

77
Q

what is the diagnosis for DIC

A

prolonged prothrombin time (bleeding time), decrease in platelets, increase in D-dimers

78
Q

what is the treatment for DIC

A

treat the underlying cause, platelet transfusion, recombinant protein C

79
Q

what is the laboratory diagnosis for an MI

A

troponin, creatine kinase, LDH

80
Q

what are the risk factors for a DVT

A

immobility, pregnancy, oral contraceptive, obesity, lack of exercise, trauma, surgery

81
Q

what is the presentation for pulmonary embolism

A

pulmonary hypertension - shortness of breath, coughing up blood, fatigue, pain

82
Q

what are the causes of fat embolism

A

fracture of long bones

83
Q

how long does it take for symptoms to appear from fat embolism

A

1-3 days to develop neurological and respiratory symptoms

84
Q

what is seen in familial hypercholesterolaemia

A

xanthoma, xanthelasma, corneal arcus

85
Q

what is a transient ischaemic attack

A

blockage of a vessel in the brain by an embolus causing pain due to lack of blood supply but the embolus quickly disintegrates so the pain then goes

86
Q

where could a clot come from to cause a TIA

A

clot could be formed from AF, an atheroma, vegetation on the heart valves

87
Q

what is the difference between ischaemic and haemorrhagic stroke

A

ischaemic - lack of blood due to blockage

haemorrhagic - blood vessel bursts giving lack of blood flow usually due to hypertension

88
Q

what is the role of atherosclerosis in TIAs

A

parts of the plaque can break off and go to the brain

89
Q

what can cause ischaemia of the bowel

A

volvulus, embolus, thrombus, adhesions (scars from surgery), hernia, atherosclerotic plaque

90
Q

what is the presentation of peripheral vascular disease

A

claudication, gangrene and necrosis of toes

91
Q

why is the lower abdominal aorta more susceptible to an aneurysm

A

there are less elastic fibres so theres less recoil making it weaker

92
Q

what are the complications of an AAA

A

rupture, death

93
Q

what is the role of atherosclerosis in an AAA

A

an atherosclerotic plaque makes the wall weaker, damaging the elastic fibres

94
Q

what are the causes of LV hypertrophy

A

aortic stenosis, hypertension, ischaemic heart disease (heart increases in size to compensate), aortic regurgitation, athletic

95
Q

what are the complications of LV hypertrophy

A

myocytes have a lack of oxygen so fibrosis occurs and they become non-functional causing death and infarct

96
Q

what is Barrett’s oesophagus

A

metaplasia of columnar psuedostratified epithelia to gastric/intestinal glandular epithelia due to acid reflux

97
Q

what are the complications of barrett’s oesophagus

A

adenocarcinoma - the metaplasia means that mutation is more likely to occur

98
Q

how can cigarette smoke cause metaplasia

A

can irritate the bronchus and airways changing the pseudostratified ciliated epithelia into stratified squamous

99
Q

what are the complications of metaplasia due to cigarette smoke

A

small cell carcinoma, squamous cell carcinoma

100
Q

what are the complications of benign prostatic hyperplasia

A

compression of the urethra

blockage of the bladder causing distension and hypertrophy therefore would need a catheter

101
Q

how does psoriasis present

A

scaly pink flakes commonly found on the elbows, knees, ears and scalp

102
Q

what is psoriasis

A

hyperplasia of keratinocytes with more keratin on top to form the flakes

103
Q

what colour infarct are MIs

A

white

104
Q

why can MIs also be a red infarct

A

due to an acute inflammatory response when new infarcts appear but they will go white over time

105
Q

what are the symptoms of an AAA

A

normally none but may get a pulsating mass in the abdomen

106
Q

what genetic disorders put you more at risk of an AAA

A

marfans and Ehlers-Danlos

107
Q

how would TB appear microscopically

A

caseating granulomas

108
Q

how would TB appear macroscopically

A

holes in apex, white patches in apex

109
Q

how would malignant mesothelioma appear macroscopically

A

thicker, white pleural sac - meaning the patient feels like they are suffocating as theie lungs cant expand

110
Q

give some causes of steatosis

A

excessive alcohol intake, obesity, hyperlipdemia, medication, diabetes, genetics

111
Q

how does a cirrhotic liver appear

A

regenerating nodules

microscopically would see blue fibrous band and red areas of regenerating cells

112
Q

what are the causes of liver cirrhosis

A

hepatitis B/C, alcohol intake, fat, toxins and medications

113
Q

what is ascites

A

accumulation of fluid in the peritoneum

114
Q

what is the main cause of ascites

A

liver cirrhosis - the liver cant produce albumin and so the osmotic pressures changes

115
Q

what is ischaemic reperfusion injury

A

when blood floe is returned to damaged tissue worsening the problem as theres more cytokines, neutrophils, and complement proteins

116
Q

how does aspirin work

A

prevents cyclooxygenase enzymes which produces prostaglandins meaning platelets cant produce thromboxane A2 which allow platelet aggregation

117
Q

how does aspirin prevent a fever

A

it prevents the production of prostaglandins which cause pain - NSAIDs also do this

118
Q

how does heparin work

A

activates antithrombin III

119
Q

how does warfarin work

A

vitamin K antagonist preventing the production of factor X

Pathology (13 decks)

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