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Year 2 Medicine Leeds > Clinical Pathology > Flashcards

Clinical Pathology Flashcards

1
Q

Name the 3 gram positive cocci and 2 gram negative cocci

A 
Positive|:
Staph aureus 
Staph pyogenes 
Streptococcus agalaitae
Negative:
Neisseria meningitides 
Neisseria gonorrhoeae
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2
Q

Name the gram positive (5) and negative (5) bacilli

A 
Positive:
Bacillus anthracis
Clostridium difficile 
Listeria monocytogenes
Corynebacterium 
Diptheriae
Negative:
Salmonella Typhi 
Shingella spp
Escherichia Coli 
Proteus spp
Yersinia pestis
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3
Q

Name the 4 gram positive coccobacilli

A

Haemophilus
Bordetella
Brucella
Pasteurella

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4
Q

Name the 5 spiral bacteria

A 
Helicobacter 
Campylobacter 
Borrielia 
Leptospira 
Treponema Pallidium
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5
Q

What does staphylococcus aureus cause?

A

Skin, soft tissue, bone infections and endocarditis

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6
Q

What does coagulase negative staphylococci cause?

A

Prosthetic device infection

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7
Q

What does streptococcus pyogenes cause?

A

Scarlet fever, sore throat, necrotising fasciitis, puerperal sepsis

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8
Q

What does streptococcus pneumoniae cause?

A

Pneumonia, meningitis

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9
Q

What does escherichia coli cause?

A

UTI’s, sepsis, intra-abdominal infections

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10
Q

What does pseudomonas aeruginosa cause?

A

Ventilator associated pneumoniae

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11
Q

What does Neisseria meningitidis cause?

A

Meningococcal sepsis, meningitis

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12
Q

What does Neisseria gonorrhoeae cause?

A

Gonorrhoea, ophthalmia neonatorum

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13
Q

What does haemophilia influenzae cause?

A

Respiratory tract infections, meningitis, epiglottitis

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14
Q

What does chlamydia trachomatis cause?

A

Chlamydia

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15
Q

What does clostridium difficile cause?

A

Pseudomembranous colitis

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16
Q

What does mycobacterium tuberculosis cause?

A

TB - pulmonary and extra pulmonary

Meningitis

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17
Q

What are the 6 stages of virus life cycle?

A
  1. Adsorption
  2. Penetration
  3. Uncoating
  4. Synthesis
  5. Assembly
  6. Release
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18
Q

Describe the herpes virus (5 Strains)

A 
Simplex 1 - coldsores 
Simplex 2 - genital 
Varicella zoster - chickenpox/shingles 
Epstein-Barr - EBV
Cytomegalovirus - CMV
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19
Q

Describe respiratory viruses (4)

A

Rhinovirus - common cold
Influenza - Flu
Covid
Respiratory syncytial virus- bronchiolitis

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20
Q

Describe hepatitis viruses mode of transmission (4)

A

Hep A +E - faeco-oral

Hep B + C - Sexual, vertical, parenteral

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21
Q

Describe GI tract transmitted viruses (3)

A

Norovirus
Rotavirus
Enteroviruses - polio, fever rash syndromes

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22
Q

Describe the 4 “childhood” viruses

A

Mumps - parotids, orchitis
Measles - encephalitis SSPE
Rubella
Parvovirus - erythema infectious

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23
Q

Describe prions viruses

A

CJD
nvCID
Both show spongiform encephalopathy
Mad Cow disease

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24
Q

Describe dermatophytes

A

originate in soil/animals or humans
Geophilic
Zoophilic
Anthropophilic

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25
Q

Describe the 5 common fungal diseases

A 
Tinea pedis - athletes foot 
Tinea unguinum - fungal nail disease 
Tinea curries - jock itch 
Tinea corporis - ringworm 
Tinea capitis - scalp ringworm
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26
Q

What is the treatment for tines capitis?

A

Systematic oral antifungals depending on cause - griseofulvin, terbinafine, itraconazole

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27
Q

What is malassezia?

A

Genus of yeasts
Part of normal skin flora
Causes pityriasis vesicolor

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28
Q

What are the 5 malaria species?

A 
Plasmodium falciparum 
Plasmodium Vivax 
Plasmodium Ovale 
Plasmodium Malariae 
Plasmodium Knowlesi
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29
Q

What is the atopic triad?

A

Eczema, asthma and rhinitis

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30
Q

What is auto inflammation?

A

Spontaneous attacks of systematic inflammation, no specific source of infection and an absence of high titre autoantibodies and antigen specific auto reactive T cells

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31
Q

What are the histamine producing cells?

A

Mast cells
Basophils
Eosinophils

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32
Q

Describe autoimmunity

A
  • T cells recognition of self antigens
  • B cells and plasma cells that make autoantibodies
  • Inflammation in target cells, tissues and organs is secondary to actions of T cells, B cells and autoantibodies
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33
Q

What are the three mechanisms of autoimmunity?

A
  1. Failure of central tolerance - T cell and B cell selection in the thymus and bone marrow retrospectively
  2. Genetic predisposition - HLA types selected for certain self antigens
  3. Antigenic factors - infections that trigger autoimmune response, environmental triggers ie. UV light, smoking etc
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34
Q

What does a non functional FoxP3 gene indicate?

A

Gene for immune system, lack of functionality indicates no functional T cells present within the immune system

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35
Q

What are the two types of autoimmune thyroid disease?

A

Hashimotos Thyroiditis - under active

Graves - overactive

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36
Q

Describe SLE (Systematic lupus erythematous)

A

Autoantibodies form against different molecules in the cell nucleus: ddDNA, dsDNA, ribosomes, histones

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37
Q

Describe sequestered antigens involved in cell death and failed clearance of nuclear antigens

A
  • Nuclear self antigens are intracellular (shielded from immune system)
  • Apoptosis clears nuclear material
  • Necrosis cell death, nuclear antigens may not be cleared and may act as antigens to the immune system
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38
Q

Describe ANA - antinuclear antibodies

A

Antibodies that bind to the cell nucleus, can be more specific and identify subtypes of antibody that bind to parts of the nucleus
- Target nucleus of cell

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39
Q

Describe anti-CCP antibody (ACPA)

A

Specific 95%, useful as a prognostic marker. Positive ACPA indicate more severe and erosive disease
- Usually used for rheumatoid arthritis

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40
Q

Describe ANCA testing

A

Pattern of autoantibody

- Suggests clinical diagnosis specifically for vasculitis

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41
Q

Describe autoantibodies in type 1 diabetes

A
  • Non pathogenic
  • Several types: islet cell antibodies, antiGAD65, antiGAD67, antiinsulinoma antigen 2 and insulin autoantibodies
  • Disappear with progression of disease and total destruction of beta islet cells Disease confirmation
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42
Q

Describe Pernicious Anaemia in relation to antibodies

A

Antigen: H+, K+ ATPase located in the gastric parietal cells of rodent stomach

  • Clinical antibody present in more than 90% of patients with pernicious anaemia
  • Autoimmune gastritis leads to pernicious anaemia which is characterised by antibodies to GPC and intrinsic factor
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43
Q

Describe defects in innate immunity

A
  • Neutrophils and macrophages
  • Pathogen recognition receptors recognise conserved pathogen associated molecular patterns (PAMPs)
  • Liposaccharide = PAMP
  • Phagocytes use PRRs to detect pathogens
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44
Q

Describe complement deficiencies

A
  • C2,C4 - SLE infections and myositis

- C5-C9 form membrane attack complex, present with repeated bacterial meningitis - Neisseria

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45
Q

Describe chronic granulomatous disease

A
  • Recurrent abscesses: lung, liver, bone, skin and gut
  • Unusual organisms e.g. staphylococcus, klebsiella, serretia, aspergillum, fungi
    Diagnosis: rely on reduction neutrophil function test or nitro blue tetrazolium dye
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46
Q

Describe defects in the adaptive immunity

A
  • Antibody production
  • B cell defects: CVID, IgA deficiency , x linked hyper IgM syndrome transient hypoglobulinaemia of infancy
  • Loss of antibody secretion
  • lead to recurrent bacterial infections
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47
Q

What is the treatment for antibody deficiency?

A

Antibiotics and immunoglobulin G replacement from blood donors

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48
Q

Describe SCID

A

Severe combined immunodeficiency disease

  • No T cells + suggestive history
  • Paediatric emergency with haemopoietic stem cell transplant as only cure
  • Antibiotics, antivirals and antifungals given as treatment
  • Causes: absence of critical T cell molecule TCR common gamma chain, loss of communication MHC2 deficiency, metabolic adenosine deaminase deficiency
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49
Q

Describe adoptive immunotherapy

A

Bone marrow transplant

Stem cell transplant, replacement of the immune system

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50
Q

Describe the drugs targeting lymphocytes

A

Antimetabolites - azathioprine, mycophenolate mofetil (MMF)
Calcineurin Inhibitors - cyclosporin A, tacrolimus
M-TOR inhibitors - sirolimus
IL-2 receptor mABs - Basiliximab, daclizumab

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51
Q

What are JAK inhibitors?

A

Newest treatment for RA working by blocking the signalling pathways, slow down the immune system and therefore reduce RA symptoms

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52
Q

Describe HLA typing

A
  • Inherit HLA type from parents
  • Each couple have 4 possible types
  • Class 1 and A antigens are the most important in relation to transplant matches
  • Serological cell based
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53
Q

Describe Complement dependent Cytotoxicity Test CDC

A

Detects complement fixing IgG/IgM HLA and non-HLAs

  • Limited sensitivity
  • Non-HLA interference
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54
Q

Describe antibody detection in transplantation

A
  • Prevents hyper acute rejection
  • Specific against donor - pre-transplant crossmatch living or cadaveric
  • Avoid aborted transplants
  • Sensitising events - previous transplant, pregnancy and blood transfusions
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55
Q

Describe acute cellular rejection (ACR)

A
  • T cell dependent, T cell immunosuppression
  • Directed against foreign HLA molecules effect of HLA mismatch
  • Typically 7-10 days after transplant
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56
Q

Describe hypogammaglobulinemias

A
  • Antibody problems
  • Congenital X linked Acquired - multiple myeloma, burns
  • Usually encapsulated bacteria pneumoniae
  • Gardia lambila
  • Treatment typically with immunoglobulins
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57
Q

What are qualitative and quantitative neutrophil defects?

A

Qualitative - chemotaxis - rare congenital inadequate signalling
Quantitative - killing power, inherited at risk of staph aureus infections - chronic granulomatous disease

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58
Q

Describe empirical therapy - neutropenic patients

A

Treatment: broad spectrum antibiotics
1st line - antipseudomonal penicillin +/- gentamicin
2nd line - carbapenem
- Often normal flora - coagulase negative staph
- Fungal infections
- Viruses - Granulocyte stimulation factors

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59
Q

What is immunomodulation?

A

The therapeutic effect that may lead to immunopotentiation, immunosuppression or induction of immunological tolerance

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60
Q

What are 4 common acute RNA viruses?

A

Influenza, measles, mumps and hepatitis A

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61
Q

What viral syndromes have vesicular rashes?

A

Chicken pox
Herpes simplex 1/2
Enterovirus

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62
Q

What viral syndromes have non vesicular rashes?

A

Measles
Rubella
Parvovirus
HHV6

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63
Q

What is the baseline treatment for herpes simplex virus?

A

Aciclovir

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64
Q

What is the treatment of hepatitis B?

A

Lamivudine and Tenofovir

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65
Q

Describe HAART Therapy

A

Highly Active Antiviral Therapy - 2 Nucleoside reverse transcriptase inhibitors and NNRTI’s
- Require life long treatment

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66
Q

What are the beta lactams?

A

Penecillins
Cephalosporins - can
Carbapenems
Monobactams

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67
Q

What beta lactam antibiotic can patients with penicillin allergies also react to?

A

Cephalosporins

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68
Q

What are the 3 groups of anti fungal cell membrane agents? + an example for each

A

Azoles - itraconazole
Polyenes - Amphotericin B and Nystatin
Allylamine - terbinafine

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69
Q

What antibiotics are best to avoid in pregnant women and why?

A

Quinolones - damage to cartilage
Trimethoprim - folic acid antagonist
Tetracyclins - stains bones/teeth + affects bone growth

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70
Q

What is the antibiotic treatment typically used for Meningitis?

A

IV Ceftriaxone

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71
Q

What is the antibiotic typically used to treat cellulitis?

A

Flucloxacillin

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72
Q

What is the typical antibiotic for treatment for necrotising fasciitis?

A

Meropenem and clindamycin

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73
Q

What are the two methods of antibiotic resistance transfer?

A

Horizontal transfer via transposons

Vertical transfer - passed via daughter cells in bacterial division

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74
Q

What is canton Valentine leucocidin staph aureus?

A

PVL - toxin produced by less than 2% of staph aureus

- Causes recurrent skin and soft tissue infections including necrotising haemorrhaging pneumonia

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75
Q

What blood test should be run for investigation of specific infections?

A 
Immunity Detection 
- IgG - previous infection 
- IgM - current infection or reactivation 
Blood cultures M, C and S
PCR and microscopy
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76
Q

Describe renal cell carcinoma + gene mutation

A

Two types - clear cell and papillary

  • Typical in 60+ males
  • VHL gene mutation
  • Common paraneoplastic syndrome
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77
Q

Describe wilm’s tumour

A

Nephroblastoma - arises from nephroblasts
Typical in children under 5
WT1 gene
Abdominal swelling and pain

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78
Q

Describe urolithiasis

A

Kidney stones - form obstruction, urinary stasis and local trauma

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79
Q

Describe vesicoureteral reflux

A

Urine flows backwards from bladder to ureter

  • Typical in under 2’s
  • Only seen those with symptoms
  • UTI due to renal stasis
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80
Q

Describe urothelial carcinoma

A

Transitional cell carcinoma arising from urothelium

  • Typically in adults over 60 and mainly males
  • Exposure to chemicals
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81
Q

Describe Neurogenic bladder

A

Inability to empty bladder
- Spastic - if damage to brain or spinal cord
- Flaccid - if damage to peripheral nerves
Stroke, MS, pregnancy, diabetes
- Lack of bladder control

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82
Q

Describe benign prostatic hyperplasia

A

Increased stroll and glandular cells - enlarged prostate
- Older men 70% by age 60
Lower urinary tract symptoms

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83
Q

Describe prostatic adenocarcinoma and its gene association

A

Cancer of prostatic epithelium

- BRCA1/2 association

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84
Q

Describe cryptorchidism

A

Undescended testis - typical in newborns

- seen more in downs syndrome and kelinfelter syndrome

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85
Q

Describe seminoma

A

Malignant neoplasm of the testis arising from germ cells in seminiferous tubules

  • Young men 25-45
  • Pain, changes in testis shape
  • Can cause gynecomastia
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86
Q

What is the typical treatment for pyelonephritis?

A

Cefuroxime, azteonam, ciprofloxacin, gentamicin

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87
Q

What is the typical treatment for prostatitis?

A

Piperacillintazobactam, ciprofloxacin and cotrimoxazole

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88
Q

Describe the common causes of chronic kidney disease

A

Diabetes and hypertension

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89
Q

Describe minimal change disease

A

Children with nephrotic and little/no decrease in renal function

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90
Q

Describe IgA nephropathy (Berger’s Disease)

A

Autoimmune
- teens with nephritic syndrome, build up of IgA in the glomeruli causing glomerulonephritis if secondary may have PMH of cirrhosis or coeliac

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91
Q

Describe Membranous nephropathy

A

Autoimmune

- Adults with nephrotic, if secondary may have PMH of hepatitis B or cancer

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92
Q

Describe focal segmental glomerulosclerosis

A

Scar tissue develops on the glomeruli

Adults with nephrotic, if secondary may have PMH of HIV or anabolic steroid use

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93
Q

Describe lupus nephritis

A

Autoimmune

  • Young woman with molar rash and other signs of lupus
  • variable types of renal presentations
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94
Q

Describe post infectious glomerulonephritis

A

Type 3 hypersensitivity reaction

- Children with impetigo or strep throat then develop nephritic syndrome

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95
Q

Describe Granulomatosis with polyangilitis - wegners

A

Autoimmune small vessel vasculitis

  • Haematuria and rapid fall in eGFR
  • Nasal and lung symptoms
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96
Q

Describe good pastures disease

A

Type 2 hypersensitivity reaction

  • Haematuria and rapid fall in eGFR
  • Haemoptysis due to lung involvement
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97
Q

What are 5 diseases with renal manifestations?

A 
Hypertension
Diabetes 
Vasculitis 
Myeloma 
Amyloidosis
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98
Q

Describe autosomal dominant polycystic kidney disease, mutation and presentation

A

PCKD - adults
- Caused by PKD1/2 mutation
Presents - ESRD, liver cysts, berry aneurysms, heart valve problems

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99
Q

Describe Autosomal recessive polycystic kidney disease

A

PCKD - children
- PKHD 1 mutation
Presents - underdeveloped lungs at birth, 1/3 die in the first month of life

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100
Q

Describe neurocrine

A

Secretion of hormones into the blood stream by neurones

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101
Q

Describe pituitary tumours

A
  • Benign adenomas

- Hormone producing cells, prolactinoma, growth hormone

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102
Q

Describe hypothyroidism

A
  • More common in women
  • Iodine deficiency
    Hashimoto’s
  • Goitre
    Insufficiency of Thyroid hormones
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103
Q

Describe hyperthyroidism

A 
Peak age - young women 30-40 yrs 
- Excess thyroid hormone 
Graves disease 
- wide eyed stare 
- Toxic nodular goitre - most patients euthyroid
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104
Q

Describe thyroid follicular carcinoma and tumour marker

A

Well differentiated malignant tumour

  • Middle Aged onset typically
  • 90% secrete thyroglobulin which can be used as tumour marker
  • Thyroid nodules
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105
Q

Describe papillary thyroid carcinoma

A
  • Younger females
  • Thyroglobulin can be used as tumour marker
    Invasion of lymphatics
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106
Q

Describe primary hyperparathyroidism

A

Aetiology - Parathyroid adenoma
Post menopausal women
- Renal stones, muscle weakness

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107
Q

Describe Cushing’s syndrome

A
  • 25-40 years
  • Common cause is oral steroids
  • ACTH dependent increase bilateral adrenal hyperplasia
  • Excess cortisol
  • Moon face, weight gain, obesity, purple striae
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108
Q

Describe conn’s syndrome

A

More prevalent in 30-50 yrs

  • Adrenal cortisol hyperplasia, adenoma, carcinoma and familial hyperaldosteronism
  • increased blood pressure, headaches, muscular weakness, muscle spasms, excessive urination
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109
Q

Describe Addison’s disease

- Triad

A
  • Adrenal insufficiency
  • Primary adrenal cortical insufficiency
  • Secondary due to failure of ACTH secretion
  • Triad of hyperpigmentation, postural hypotension and hyponatraemia
  • Lethargy, depression, low mood, anorexia etc
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110
Q

Describe pheochromocytoma and neuroblastoma

A 
Pheochromocytoma - adults 
Neuroblastoma - children 
- Adrenal medullary tumour of neuroendocrine chromaffin cells 
- Episodic release of catecholamines 
- Hypertension, sweating, pallor
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111
Q

Describe insulinoma

A

More common in 40-60yrs

  • tumour arising from islets of langerhan
  • test for hypoglycaemia to confirm
  • Weakness, fatigue, vision problems
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112
Q

What are the function of osteoblasts?

A

Create and repair new bone, make osteoid, become osteocytes

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113
Q

What is the function of osteoclasts?

A
  • Breakdown of old bone

- Large and found in bone pits

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114
Q

What is the function of osteocytes?

A
  • Communication between osteoblasts and osteoclasts

- Crucial for bone remodelling

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115
Q

Describe investigations for bone disease

A

DEXA - bone density scan

  • ALP
  • Bone resorption
  • Bone formation
  • Osteoclast enzymes
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116
Q

Describe P1NP - pro collagen type 1 propeptides

A
  • Synthesised by osteoblasts
  • Precursor molecule of type 1 collagen
  • Serum concentration not affected by food intake
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117
Q

Describe osteoporosis

A
  • Decreased bone mass - Deranged bone micro architecture

- FRAX calculation tool for fracture risk calculations

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118
Q

Describe Paget’s disease

A
  • Rapid bone turnover and abnormal bone remodelling
  • Males over 50
  • Commonly affects pelvis, femur and lower lumbar vertebrae
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119
Q

Describe osteomalacia

A
  • Lack of mineralisation of bone
  • Widened osteoid seams with lack of mineralisation in adults
  • Widened epiphysis and poor skeletal growth in children
  • Insufficient calcium absorption from intestine and renal phosphate excretion
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120
Q

Describe bisphosphonates

A

Help to reduce bone thinning
- Mimic pyrophosphate structure
- Taken up by skeleton
Ingested by osteoclasts

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121
Q

Describe hypocalcaemia indicates

A
  • EDTA contamination
  • Vitamin D deficiency
  • Inadequate dietary calcium intake
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122
Q

What can hypercalcaemia indicate (4)

A
  • Hyperparathyroidism
  • Malignancy
  • Medications
  • Vitamin D excess
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123
Q

Describe hypomagnesaemia

A
  • Prevalent in hospitalised patients
  • Associated with hypokalaemia, hyponatraemia, hypophosphatemia and hypocalcaemia
  • Due to inadequate intake, renal loss, GI loss, redistribution into cells
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124
Q

Describe fibrocystic disease

A
  • Ages 20-45
  • Benign hormonally mediated breast changes
  • Mild epithelial hyperplasia
  • Premenstrual painful breasts
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125
Q

Describe fibroadenoma

A
  • Common 20-30 yrs
  • Mobile painless well defined breast lesion
  • Asymptomatic unless infarction occurs
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126
Q

Describe breast cancer

A
  • Late menopausal women
  • Arises anywhere in breast parenchyma or accessory breast tissue
  • Linked to oestrogens as cause
  • Palpable lump
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127
Q

Describe DCIS (Ductal Carcinoma in situ)

A

Malignant clonal proliferation of cells within breast parenchyma
- Precursor of invasive carcinoma

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128
Q

What is the most and least common breast cancer?

A

Ductal - most common
Lobular - relatively common
Metaplastic and mucinous - rare

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129
Q

What markers are used for invasive tumours?

A

ER, PR and Her 2

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130
Q

Describe endometriosis

A
  • Ectopic endometrial tissue
  • 30-40 years
  • Bleeding into tissues, fibrosis, NSAIDs
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131
Q

Describe endometrial polyps

A
  • Sessile/polypoid endometrial overgrowths
  • 40-50 years
  • Risk increases with age
  • asymptomatic, intramenstrual/postmenopausal bleeding, menorrhagia, dysmenorrhoea
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132
Q

Describe endometrial hyperplasia

A
  • Hyperplasia of the endometrium
  • > 40 years
  • Situations of oestrogens and low progesterone
  • Abnormal bleeding, IMB, PMB and amenorrhea
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133
Q

Describe endometrial cancer

A
  • Adenocarcinomas
  • Endometrioid - pre/post menopausal or serous - postmenopausal
  • Most common cancer of female genital tract
  • Features of advanced metastatic disease
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134
Q

Describe myometrial tumours

A
  • Smooth muscle tumour of myometrium
  • Commonest gynaecological condition
  • benign monoclonal proliferation of smooth muscle cells
  • Later reproductive life, irregular bleeding
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135
Q

Describe PCOS

A
  • Endocrine disorder characterised by hyperandrogenism, ovulatory dysfunction, menstrual regularities, insulin resistance
  • 6-10% of women reproductive age
  • Hirsutusm - hair on chin
  • Male pattern baldness
  • Lack of ovulation
  • Infertility
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136
Q

Describe Lynch syndrome in relation to women health

A
  • Hereditary non polyposis colorectal cancer

- Women with Lynch syndrome have a higher lifetime risk of endometrial cancer

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137
Q

Describe insulin resistance

A

Insulin receptors in theca cells respond to insulinaemia in T2DM - making them bigger, driving more LH receptors on the theca cells
Hypothalamus responds by producing more GnRh from pituitary

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138
Q

What are the two main intra-amniotic infections?

A

Chorioamnionitis - inflammation of umbilical cord, amniotic membranes/fluid/placenta
Puerperal Endometriosis - infection of the uterine lining

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139
Q

What are the main infections in children?

A
  • Neonatal sepsis
  • Respiratory tract infections - cold, tonsillitis, pneumonia, acute otitis media
  • Meningitis
  • UTI
  • Rashes associated with infections - scarlet fever, impetigo etc
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140
Q

What are the different cells in myeloid and lymphoid lineages?

A

Myeloid: granulocytes, erythrocytes and platelets
Lymphoid: B and T lymphocytes

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141
Q

Describe the granulocytes - leukocytes

A 
Neutrophils:
- Phagocytes - most common WBC
- Increased Number = neutrophilia 
- Decreased Number = neutropenia 
- Live for a few hours in blood 
Eosinophils 
- Increased - eosinophilia 
- parasitic infection and allergic reactions
142
Q

Describe monocytes

A
  • Phagocytic antigen presenting cells
  • Migrate to tissues and are identified as macrophages or histocytes
  • Kupffer cells in liver
  • Langerhan cells in skin
143
Q

Describe the lymphocytes

A 
T cells 
- adaptive immunity 
B cells 
- Rearrange immunoglobulin genes to enable antigen specific antibody production 
- Can indicate infection and myeloma if high numbers 
NK Cells 
- Innate immune system 
- Large granular lymphocytes 
- Recognise non-self cells and viruses
144
Q

What is microcytic hypochromic anaemia and its causes?

A

MCV<80 fl
MCH <27
Iron deficiency, thalassaemia, anaemia of chronic disease, Lead poisoning

145
Q

What is normocytic normochromic anaemia and its causes?

A

MCV 80-95 fl
MCH >27
- Normal haemoglobin in RBC but low amount of RBc
Many haemolytic anaemia
- Anaemia of chronic disease, after acute blood loss, renal disease, mixed deficiencies, bone marrow failure

146
Q

Describe macrocytic anaemia and its causes?

A

MCV>95
Megaloblastic:vitamin B12 or folate deficiency
Non-megaloblastic: alcohol, liver disease, myelodysplasia, aplastic anaemia

147
Q

What is tested in a full blood count?

A 
Hb
MCV
MCH
Reticulocyte count 
WCC 
Plt
148
Q

Describe 1 unit of RBC transfusion

A
  • Raises Hb by 10g/L
  • 200-250mg iron
  • Stored at 4 degrees for up to 35 days
  • 280 ml
  • Dose 10-20ml per 1kg
149
Q

Describe FFP

A
  • Contains all clotting factors at physiological levels
  • 12-15ml/kg - 4 units
  • 1 unit = 300ml
  • Stored at -30 degrees
150
Q

What is cryoprecipitate?

A
  • Extracted from FFP during thawing process
    Contains: fibrinogen, von Willebrand factor VII and XII
  • 10-15ml/kg - 10 units typically
151
Q

Describe platelets used for transfusions

A
  • Raise count by 20-60x10^9/L
  • 1 unit platelets from 1 unit whole blood
  • 4-6 units pooled together into a single pack - can be from different donors
  • Stored at room temp for up to 5 days on an agitator
152
Q

What is TRALI?

A 
Transfusion related acute lung injury 
- serious complication of transfusion 
- Due to antibodies in the transfused unit against antigen expressed on recipients leukocytes 
- Acute lung injury 
Plasma used from male donors only in uk
153
Q

What is Von Willebrand disease?

A
  • Most common heritable bleeding disorder
  • Autosomal dominant inheritance
  • Reduction in factor VII
    Treatment - antifibrinolytics - transexamic acid
154
Q

Describe haemophilia A and B and treatment

A

A = Factor VIII deficiency
B = Factor IX - expressed in males and carried by females (Typically)
Treatment - replacement of missing clotting factor

155
Q

What is emicizumab (hemlibra)?

A
  • Monoclonal antibody
  • Replace the action of missing FVIII in the clotting cascade
  • Binds to Factor IXa and X forming a link between the factors
  • Factor IXa activates FX allowing clotting cascade to continue
156
Q

What is the main difference between low molecular weight heparin and unfractionated heparin ?

A

LMWH - switches off factor Xa

Unfractionated - switches off factor Xa and thrombin

157
Q

What is vitamin K deficiency caused by and treatment?

A
  • Obstructive jaundice
  • Prolonged nutritional deficiency
  • Broad spectrum antibiotics
  • Neonates
    Treatment: IV/oral vitamin k 10mg for 3-5 days
158
Q

What is HIT and treatment?

A

Heparin induced thrombocytopenia

  • Dropped platelet count >50% from baseline
  • usually 5-10 days after starting heparin
  • stop heparin treatment and start argatroban
159
Q

What is fondaparinux?

A
  • Synthetic pentassaccharide given subcutaneously

- Binds antithrombin and inhibits Xa activity

160
Q

What is aspirin?

A

Antiplatelet

  • inactivates platelet cyclooxyrgenase reducing thromboxane A2
  • Irreversible affects lasting 4-5 days
161
Q

What are the 3 P2Y 12 antagonists, their effect time, half life and action?
(Antiplatelets)

A 
Clopidogrel 
- 4-8 hours for effect 
- 0.5 hours half life 
- 5-7 days action
Prasugrel 
- 2-4 hours for effect 
- 7 hours half life 
- 5-7 days action 
Ticagrelor 
- 2-4 hours for effect 
- 8-12 hours half life 
- 3-5 days action
162
Q

What is the major haemorrhage protocol?

A
  • HR>110, systolic BP<90mmHg
  • Transfusion of a volume equal to then patients total volume in less than 24 hours
  • Transexamic acid 1g bolus over 10 mins followed by IV 1g over 8 hours
163
Q

What is disseminated intravascular coagulation + treatment?

A
  • Clinicopathological syndrome complicating a range of illnesses
  • Systematic activation of pathways leading to and regulating coagulation which can result in the generation of fibrin clots that may cause organ failure
  • Consumption of platelets can lead to increased bleeding risk
    Treatment:
    Antibiotics
    Obstetric Intervention
    Maintain tissue perfusion
164
Q

Describe physiological anaemia and macrocytosis in relation to pregnancy

A

Anaemia
1st and 3rd Trimester Hb<110g/L
2nd Trimester Hb<105
- Gestational thrombocytopenia

165
Q

What are the differences in RBC mass and plasma volume during pregnancy?

A

RBC - increases by 25%

Plasma - 50% increase in volume

166
Q

What is sickle cell trait?

A
  • Heterozygous
  • Normal blood count
  • Clinically no problems except when extreme hypoxia/dehydration
  • Long fibrils distort red cell membrane - short lifespan
167
Q

What is sickle cell disease and treatment?

A 
- Homozygote 
Blood count - anaemia  Hb 60-80g/L
- Presentation occurs in infancy as foetal haemoglobin decreases
Treatment:
Penicillin from 6 months 
Transfusions, Hydroxycarbamide 
Bone marrow transplant
168
Q

What are the three types of thalassaemia and treatment?

A

Alpha - most serious, both Hb A and F have alpha chains
Beta - reduced rate of production of beta-globin chains
Total Hb level normal or only slightly low
Intermedia - no requirement for regular transfusions in first 3-5 years of life
- Bone changes and osteoporosis

Treatment:

  • Transfusion
  • Suppression of marrow red cell production and prevention skeletal deformity and liver/spleen enlargement
  • Iron chelators - promote excretion of iron in urine
169
Q

Describe haemoglobin in each trimester of pregnancy

A

1st - gamma and Portland
2nd - Foetal Hb
3rd - more adult Hb A2 and some foetal

170
Q

What are the primary and secondary immune disorders causing acquired bleeding and bruising in children?

A 
Primary 
- Thrombocytopenia 
- TTP 
Secondary 
- SLE 
- ALPS - autoimmune lymphoproliferative syndrome
171
Q

What is pernicious anaemia?

A
  • Caused by B12 deficiency

- Parietal cells of stomach

172
Q

What is subacute combined degeneration of the cord, presentation and treatment? (SACDC)

A 
Myelin sheath deteriorates on spinal cord due to B12 deficiency 
Any cause of B12 deficiency 
- Anaemia not an absolute requirement 
Presentation:
- Peripheral neuropathy
- Numbness and distal weakness 
- Unsteady walking 
- Dementia 
Treatment:
B12 and folate, folic acid
173
Q

What is immune thrombocytopenia purpura (ITP) presentation and treatment?

A
  • Immune disorder that occurs on its own or as part of another immune disorder - decreased platelets in the blood
  • Can be acute, chronic or relapsing
    Presentation:
  • Bruising, petechiae, bleeding
    Treatment
  • Steroid
  • IV immunoglobulins
  • New thrombocytopenia-mimetics
174
Q

What is May Thurner syndrome?

A

Anatomical variant in which the right common iliac artery overlies and compresses the left common iliac vein against lumber spine
- Rare cause of iliofemoral DVT

175
Q

What are the inherited forms of hyper coagulability? (4)

A
  • Factor 5 Leiden
  • Prothrombin gene mutation
  • Protein C and S deficiency
  • Antithrombin deficiency
176
Q

Describe acute leukaemia

A
  • Results of accumulation of early myeloid (AML) or lymphoid (ALL) precursors in the bone marrow, blood and other tissues
  • Somatic single cell mutation within a progenitor cell population
177
Q

What is acute myeloid leukaemia (AML)?

A 
Most common acute leukaemia in adults 
FLT3 mutation 
Median age 69 years 
Presentation:
- anaemia, infections, fatigue, haemorrhage 
Treatment:
Intensive chemotherapy 
Relapse - typical within 18 months of chemotherapy stopping
178
Q

What is intensive chemotherapy?

A

Immediate treatment

Critically ill patients with rapidly progressive disease

179
Q

What is acute lymphoblastic leukaemia (ALL)?

A
  • Most common blood cancer typically in children
  • Philadelphia chromosome association
    Presentation: fatigue, bruising, bleeding, weight loss, night sweats
    4 treatment components
    1. Induction 8 weeks
    2. Intensification 4 weeks
    3. Consolidation 20 weeks 4. Maintenance 2 years
180
Q

What is neutropenic sepsis?

A

Life threatening complication of chemotherapy
Fever, hypotension, organ impairment
Treatment - broad spectrum antibiotics

181
Q

What is myelodysplasia (MDS)?

A
  • Several related disorders with common features
  • Clonal bone marrow stem cell disorders that result in ineffective haematopoiesis with reduced production of one or more of peripheral blood cell lineages
182
Q

What is polycythaemia vera?

A

Type of blood cancer - bone marrow makes too many RBC
All ages - peak 50-70 yrs
- Itching, plethoric face, headaches
- JAK2 mutation - EPO receptor switched on continuously
Treatment - blood withdrawals

183
Q

What are the three chronic myeloproliferative disorders?

A

Polycythaemia Vera
Essential Thrombocytosis
Idiopathic Myelofibrosis

184
Q

What is chronic myeloid leukaemia?

A
  • Very high white cell count
  • Median age 55-60
  • Increase leukocytosis
  • Philadelphia chromosome
  • Weight loss, fever, fatigue, bleeding, bruising
185
Q

Describe myeloma pathophysiology etc

A
  • Malignant disorder of clonal plasma cells
  • 70 years
  • Presentation - confusion, poor appetite, thirst, bone pain, nausea
  • CRAB features
  • Management of acute kidney injury
  • Management of acute kidney injury, steroids, individualised therapy
186
Q

Describe Hodgkin lymphoma pathophysiology etc

A

Presence of Hodgkin reed-stern berg cells within a cellular infiltrate of non-malignant inflammatory cells

  • Age 20-40 and over 75
  • Breathlessness, night sweats, itching
  • Chemo and radiotherapy
187
Q

Describe non-hodgkin lymphoma pathophysiology etc

A

Follicular lymphoma, neoplastic disorder of lymphoid tissue

  • Arises with age
  • Slowly enlarging lymph nodes
  • chemotherapy
188
Q

Describe chronic lymphocytic leukaemia pathophysiology etc

A

Malignant disorder of mature B cells
Most common Leukaemia in UK
- Age - over 60’s
- Lymphocytosis, lymphadenopathy, splenomegaly
- Monitoring if caught early, chemotherapy
Binet staging
A + B = normal levels of platelets and Haemoglobin
C = low levels of haemoglobin and platelets

189
Q

What are CRAB features?

A

C - hypercalcaemia
R - renal insufficiency
A - anaemia
B - bone lesions

190
Q

Describe lymphomas

A
  • Caused by malignant proliferations of lymphocytes B or T cells
  • Lymph nodes predominantly affected
191
Q

What is thrombotic thrombocytopenia purpura (TTP)?

A
  • Microangiopathic haemolytic anaemia
  • Red cells torn apart during circulation
    Reduced activity of ADAMTS13 enzyme - accumulation of ultra large von willebrand factor molecules - intravascular thrombosis
  • Confusion, seizures, strokes, fever, renal failure
    Treatment: urgent plasma exchange, suppress antibody production - steroids
192
Q

Describe spinal cord compression in relation to haematology

A
  • Steroids to reduce tumour size

- Likely cause is myeloma

193
Q

Describe superior vena cava obstruction haematological emergency

A
  • Pressure from mass obstructing the superior vena cava
    Causes - face and upper limb swelling, breathlessness, headaches etc
  • Steroids to reduce swelling
  • Likely cause is Hodgkin lymphoma
194
Q

What is CAR-T therapy?

A
  • Genetically modifying patients own T cells
  • Activates T cells and redirects them towards cancer cells
  • Current treatment for leukaemia and lymphomas
195
Q

What is tumour lysis syndrome?

A
  • Rapid breakdown of tumour cells - release of potassium and phosphate, elevated uric acid
  • leads to renal failure, cardiac arrhythmia
    Treatment: IV fluids, dialysis
196
Q

What is cytokine release syndrome?

A
  • Exaggerated physiological response to immune therapies in release of inflammatory cytokines
  • High fever, hypotension, hypoxia
    Treatment: broad spectrum antibiotics, IV fluids, oxygen
197
Q

What is immune cell related neurological toxicity?

A
  • Occurs at the same time or just after cytokine release
  • Wide range of neurological symptoms including confusion, seizures and coma
  • Steroids to suppress immune cells
  • Neurological assessments using the ICE and ICANS scores
198
Q

What is the definition, aetiology, epidemiology, pathogenesis, morphology and clinical features of asthma?

A
  1. Reversible intermittent narrowing of conducting airways
  2. Allergens, drugs (NSAIDs), cold exercise
  3. Children and young adults - atopic
    Adults - non atopic
  4. Sensitisation to trigger followed by re-exposure to trigger
  5. wall = thick contracted lumen mucus
  6. SOB, wheeze, cough, hyperinflation
199
Q

What is the definition, aetiology, epidemiology, pathogenesis, morphology and clinical features of COPD?

A
  1. Combination of chronic bronchitis and emphysema
  2. Tobacco smoke
  3. Long standing cigarette smokers
  4. Chemicals and heat trigger inflammation in bronchi and lung parenchyma - persistent inflammation and scarring
  5. Bronchitis emphysema alveolar wall loss especially around bronchioles
  6. SOB, inflammation of mucus secretion, coughing, mucus production
200
Q

What is the definition, aetiology, epidemiology, pathogenesis, morphology and clinical features of bronchiectasis?

A
  1. Permanent dilation of bronchi and bronchioles due to wall damage, secondary to necrotising infection
  2. Mainly obstructive or infective
  3. Dependent on cause
  4. Obstruction causes infection, inflammation damages wall tissues, walls dilate but contain inflammatory debris and mucus
  5. Dilated inflamed airway walls
  6. Productive cough, obstructive ventilatory defects, repeated infections
201
Q

What is the definition, aetiology, epidemiology, pathogenesis, morphology and clinical features of idiopathic pulmonary fibrosis?

A
  1. Progressively patchy scarring especially in lower zones of both lungs that is fatal
  2. Idiopathic
  3. > 60 years
  4. Speculated is repeat epithelial injury leading to inflammation and fibrosis
  5. Patchy interstitial fibrosis especially lung bases at periphery
  6. Insidious dry cough and progressive SOB
202
Q

What is the definition, aetiology, epidemiology, pathogenesis, morphology and clinical features of pneumoconiosis?

A
  1. Lung damage secondary to particle inhalation commonest = coal dust/silica from mining, asbestos
  2. Chronic particle inhalation
  3. More male due to occupational exposures as does dependent often older
  4. Particles ingested by macrophages, trigger fibrosis
  5. Dust accumulation and fibrosis often centred on smaller conducting airways
  6. Slowly increasing SOB
203
Q

What is the definition, aetiology, epidemiology, pathogenesis, morphology and clinical features of sarcoid ILD (Interstitial lung disease) ?

A
  1. Multisystem granulomatous disease that most commonly involves lymph nodes and lungs
  2. Idiopathic
  3. All ages 20-60
  4. Granulomatous inflammation leads to fibrosis
  5. Non-caseating granulomas in multiple sites often scarring
  6. Nodal enlargement respiratory symptoms
204
Q

What is the definition, aetiology, epidemiology, pathogenesis, morphology and clinical features of hypersensitivity pneumonia?

A
  1. Inflammatory and fibrotic bronchiolar response to inhaled antigens
  2. Inhaled
  3. Dependent on trigger
  4. Hypersensitivity response to antigen in wall of bronchioles, inflammation triggering fibrosis if antigen not removed
  5. Chronic inflammation around bronchioles spilling out into interstitium - interstitial fibrosis
  6. Respiratory symptoms
205
Q

What is the definition, aetiology, epidemiology, pathogenesis, morphology and clinical features of cystic fibrosis?

A
  1. Disease from abnormally thickened mucus
  2. Chloride channel recessive gene
  3. 1 in 2500
  4. Reduced sodium and chloride in lumen of respiratory tract, GI and seminiferous tubules - causes dehydrated mucus which is thicker and blocks lumina
  5. Lung infections, bronchitis, pancreatic exocrine atrophy
  6. Depends on predominant organ involvement
206
Q

What are the 4 chronic interstitial lung diseases?

A

Idiopathic pulmonary fibrosis
Pneumoconiosis
Sarcoid
Hypersensitivity pneumonia

207
Q

Describe the epidemiology, aetiology, pathogenesis, clinical features and non specific effects of lung cancer

A
  1. Most common cause of cancer death in UK, 40-70 years
  2. Tobacco smoking, lung fibrosis, EGFR, KRAS, ALK, ROS1
  3. Oncogenic drivers, squamous cell carcinoma
  4. Local effects of tumour, distant metastases
  5. Usually metabolic effects, weight loss lethargy, electrolyte disturbances, clubbing
208
Q

What are 4 possible causes of acute sore throat and a brief description of each?

A

Pharyngitis - inflammation of the back throat resulting in sore throat and fever
Acute tonsillar pharyngitis - symmetrically inflamed tonsils and pharynx
Infectious Mononucleosis - symmetrically inflamed tonsils/soft palate inflammation and posterior cervical lymphadenopathy
Epiglottitis - sudden onset of sore throat and fever, inflammation of the epiglottis and surrounding tissue leading to airway obstruction

209
Q

What is the cause of infectious mononucleosis/glandular fever?

A

Epstein Barr virus

210
Q

What is otitis externa, subtypes and management?

A
  • Inflammation of the external ear canal
  • Topical agents for mild/moderate and topical plus systematic antibiotic such as flucloxacillin for severe
    Malignant - external otitis spreading to the skull base
    Chronic - Often bilateral, canal wall thickening narrowing external ear canal - allergic contact dermatitis
211
Q

What is otitis media?

A

Middle ear inflammation
Fluid in middle ear
Common in children
Caused by - streptococcus, pneumonia, haemophilia influenza
Possible complications with the mastoid bone and air cells

212
Q

What is pinna cellulitis + antibiotics used for treatment?

A
  • Acute ear injury/ soft tissue
  • Associated with trauma, surgery or burns
  • Infective agents:pseudomonas aeruginosa/ staph aureus
  • Treat with ciprofloxacin and flucloxacillin
213
Q

What is aspergillosis?

A
  • Infection caused by common mould
  • Immunocompromised patients and those with lung disease are at higher risk of developing health issues related to mould
  • Allergic reactions, infections
214
Q

What is nocardia asteroides + antibiotic treatment?

A
  • Nocardia is a genus of bacteria found in the environment
  • Pulmonary nocardiasis is acquired through inhalation
  • More common in the immunosuppressed and those with pre-existing lung disease
  • Development of lung abscess
    Treatment: supportive Rx(ABC), antibiotics - co-trimoxazole
215
Q

What is a pulmonary aspergilloma ?

A
  • Mobile mass of aspergilus within a pre existing lung cavity
  • Cough, haemoptysis, wright loss, wheeze and clubbing
    Treatment: 10% cases resolve spontaneously, surgical resection, antifungals
216
Q

What is mycobacterium tuberculosis?

A
  • Infection acquired by inhalation of infected respiratory droplets, bacilli lodge in alveoli and multiply resulting in ghon focus
  • Pulmonary tuberculosis is the most common presentation
  • Can disseminate or affect almost any other organ
  • Diagnosis: clinical features, supportive radiology, detection of acid-fast bacilli or culture of M.tuberculosis from specimen
    Treatment: combined chemotherapy for several months
    Prevention: BCG to infants and children in high prevalence areas
217
Q

Describe normal mesothelium

A

A single layer of mesothelial cells lining the pleural cavity, secrete hyaluronic acid rich mucinous pleural fluid that lubricates the fluid

218
Q

Describe pleural fibrosis

A
  • Usually secondary to pleural inflammation
  • Unilateral or bilateral
  • Widespread thick fibrosis preventing normal expansion and compression of the lung causing breathlessness
219
Q

Describe parietal pleural fibrous plaques

A
  • Associated with low levels of asbestos dust exposure
  • Usually bilateral
  • Asymptomatic
  • May be visible on chest radiographs
  • Dense poor cellular collagen
220
Q

Describe diffuse pleural fibrosis

A
  • Associated with high levels of asbestos
  • Usually bilateral
  • Dense cellular collagen not extending into interlobular fissures
  • Prevents normal expansion of the lung
221
Q

Describe pleural effusions and the two main types

A

Build up of fluid between pleura:
Transudates -
- Low capillary oncotic pressure and/or high hydrostatic pressure
- Intact capillaries
- low amount of protein and lactate dehydrogenase

Exudates
- Capillaries lose semipermeability
- Normal oncotic pressure and vascular hydrostatic pressure
- High protein and lactate dehydrogenase
- Inflammation without infection
Symptoms
- Breathlessness
- Little/no pleuritic pain
Signs
- Dull percussion
- Reduced breath sounds on auscultations
Treatment
- Treat the breathlessness by removing fluid
- Identify and treat underlying cause

222
Q

What are the types of pneumothorax, causes, diagnosis and treatment?

A

Open
- Chest wall perforation usually traumatic
- External air drawn into pleural cavity
Closed
- Ruptured emphysematous bull
- Common inflammatory lung disease
- Can be traumatic - lung tears from fractured ribs
Tension
- Perforation into pleural cavity allowing air into the cavity but not out
- Pressure rises and can compress mediastinal structures
Diagnosis
- Signs - cyanosis, tachycardia, contralateral tracheal deviation in tension pneumothorax
Treatment
- May resolve spontaneously
- Decompression via needle aspiration
- Chest tube

223
Q

Describe malignant mesothelioma

A

Neoplasm of mesothelial cells that line serous cavity
- Tend not to metastasise widely
- Mixed tubulopapillary epithelioid and spindle cell sarcomatous morphology
Causes:
- Asbestos
- Thoracic irradiation
- BAP1 mutations - gremlin mutations in familial cancer syndrome with uveal melanomas and mesotheliomas

224
Q

What is left sided hypertensive heart disease?

A
  • Left ventricular concentric hypertrophy

- History or pathological evidence for hypertension

225
Q

What is right sided hypertensive disease - Cor Pulmonale?

A
  • Right ventricular hypertrophy, dilation and potentially heart failure secondary to pulmonary artery hypertension caused by disorders of the lung or pulmonary vasculature
226
Q

What are true and false aneurysms?

A

True - when bounded by arterial wall components or the attenuated wall of the heart
False - Breach in the vascular wall leading to an extravascular haematoma that freely communicated with intravascular space

227
Q

Describe the definition, epidemiology, aetiology, pathogenesis and clinical features of left sided heart failure

A
  1. Syndrome resulting from insufficient left ventricular output
  2. 1% above 75
  3. Ischaemic, hypertensive and valvular heart disease
  4. Low CO - low BP sympathetic overdrive and renin angiotensin activated
  5. Dyspnoea, fatigue and palpitations, peripheral oedema and ascites,
    - Poor prognosis - 3 years
228
Q

Describe the definition, epidemiology, aetiology, pathogenesis and clinical features of right sided heart failure

A
  1. Insufficient right ventricular output
  2. uncommon
  3. Lung diseases, ischaemic heart disease
  4. Pulmonary hypertension - increased workload of right ventricular hypertrophy
  5. SOB, peripheral oedema
229
Q

What are the 4 valvular heart diseases?

A

Aortic stenosis, aortic regurgitation, mitral stenosis, mitral regurgitation

230
Q

Describe the definition, epidemiology, aetiology, pathogenesis and clinical features of aortic stenosis

A
  1. Narrowing of aorta
  2. Most common VHD
  3. Senile calcific aortic stenosis, congenital bicuspid valve, chronic rheumatic disease
  5. Chest pain, syncope, SOB
231
Q

Describe the definition, epidemiology, aetiology, pathogenesis and clinical features of aortic regurgitation

A
  1. Dilation of root of aorta
  2. Common secondary to rheumatic heart disease + bacterial endocarditis
  4. Marfans syndrome, ankylosing spondylitis, congenital leaflet abnormalities
232
Q

Describe the definition, epidemiology, aetiology, pathogenesis and clinical features of Mitral stenosis

A
  1. Narrowing of mitral valve
  2. Reduced blood flow increases pressure in left atrium - pulmonary oedema and dyspnoea
  3. Increased risk of atrial fibrillation
233
Q

Describe the definition, epidemiology, aetiology, pathogenesis and clinical features of mitral regurgitation

A
  1. Common due to mitral valve prolapse or ischaemic heart disease or infective endocarditis
  2. One leaflet prolapses into the left atrium during systole
  3. Patients may remain asymptomatic but eventually left ventricular failure occurs
234
Q

Describe the definition, epidemiology, aetiology, pathogenesis and clinical features of ASD

A
  1. Abnormal hole in atrial septum - most common away from valve - foramen ovale
  2. Mainly paediatric
  3. causes left to right shunt, SOB
235
Q

Describe the definition, epidemiology, and clinical features of VSD

A
  1. Most common hole in inter ventricular septum mostly in upper part
  2. Paediatric
  3. Risk of endocarditis - causes left to right shunting
236
Q

Describe the definition, epidemiology, aetiology, pathogenesis and clinical features of coarctation of the aorta

A
  1. Narrowing of the aorta - birth defect
  2. Paediatric and adult
  3. Child - allows cardiac output to body via ductus arteriosus
    Adult - delayed pulse in lower limbs
  4. Cyanosis in lower half of body
237
Q

Describe the definition, epidemiology, aetiology, pathogenesis and clinical features of tetralogy of fallot

A
  1. Congenital heart defects affecting normal blood flow
  2. Pulmonary stenosis, VSD, right ventricular hypertrophy, displacement of aorta over VSD
  3. causes right to left shunting
238
Q

Describe the definition, epidemiology, aetiology, pathogenesis and clinical features of giant cell arteritis

A
  1. Vasculitis of large arteries in head
  2. Caucasian women > 50
  3. Type 4 hypersensitivity
  4. Inflammatory infiltrate narrow vessels - ischaemia
  5. Jaw claudication, blindness, flu like symptoms
239
Q

Describe the definition, epidemiology, aetiology, pathogenesis and clinical features of rheumatic fever

A
  1. Complications of strep throat mainly affecting heart especially the mitral valve
  2. Children in developing countries
  3. Strep A pyrogens
  4. Antibody cross reactivity between bacterial M protein and host tissues
  5. Mitral stenosis, erythema marginatum sydenhams chorea, arthritis, fever
240
Q

What is the aetiology and diagnosis of infective endocarditis?

A

Staph aureus + epidermidis, strep viridian’s + bovis

Diagnosis - echocardiography + 3 sets of blood cultures at different times

241
Q

What are the 4 cardiomyopathies, epidemiology and their pathogenesis?

A 
Dilated 
- Males 20-50 
- Pump failure to empty 
Hypertrophic 
- All ages and genders 
- Pump failure to empty or fill 
Restrictive 
- Dependent on cause 
- Pump failure to fill 
Arrhythmogenic 
- Most common in young males 
- Pump failure to empty
242
Q

What are the 6 Ps in Acute Peripheral vascular disease?

A
  1. Pale
  2. Pulseless
  3. Painful
  4. Paralysed
  5. Paraesthetic
  6. Perishingly cold
243
Q

What are the common bacteria causing bacterial meningitis for <1 month, 1-23 months, 2-50 years and >50 years of age?

A

<1 month - strep agalicitae, e.coli, listeria monocytogenes
1-23 - strep pneumoniae, neisseria meningitis
2-50 - strep pneumoniae, N . meningitides
>50 years - strep pneumoniae, N. meningitis’s, listeria monocytogenes

244
Q

What are the common causative agents and presentation for viral meningitis?

A

Enteroviruses - echo, coxsackie A, B
Herpes simplex, varicella zoster
Respiratory or intestinal infection - CSF shows raised lymphocyte count

245
Q

What are the bacteria typically causing brain abscesses?

A 
Streptococci
Staph aureus - most common post surgery 
Bactericides 
Pseudomonas 
E.coli
246
Q

What are the 4 phases of rabies infection and their associated symptoms/presentation?

A
  1. Prodromal Phase - fever, nausea, vomiting, headache
  2. Furious Phase - agitation, disorientation, seizures
  3. Dumb Phase - paralysed, stuporous
  4. Coma Phase - death
247
Q

What is the main class of antibiotics to treat meningitis and what bacterial meningitis does it not treat?

A

Cephalosporins

Does not treat listeria causing meningitis

248
Q

What are the three classifications of meningitis?

A

Acute pyogenic - usually bacterial
Aseptic - usually viral with lymphocytic pleocytosis
Chronic - mycobacterium tuberculosis, spirochetes, cryptococcus neoformans

249
Q

What medication is given to suspected meningitis patients prior to antibiotic treatment?

A

Steroids - dexamethasone

Given for 4 days with pneumococcal meningitis specifically

250
Q

What are the 4 mechanisms of spread of meningitis?

A

Haematogenous
Direct implantation
Local extension
Along peripheral nerves

251
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features and treatment for oral lichen planus?

A
  1. Non infectious inflammatory condition
  2. Females
  3. Immune
  4. Cell mediated immune response
  5. Erythmatous, erosive
    Wickham striae - intercalating what striae
    Itchy skin
  6. Topical steroids
252
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features and treatment for epiglottitis?

A
  1. Swelling of the epiglottis
  2. Anyone
  3. Capsulated form of haemophilus influenzae B
  4. Leads to airway obstruction
  5. Sore throat, breathing difficulties, dysphagia
  6. Intubation, tracheostomy, antibiotics
253
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features and treatment for Allergic laryngitis?

A
  1. Inflammation of the larynx
  2. Anyone
  3. Inhalation of allergens/irritants
  5. Sore throat, hoarseness
    Can lead to obstruction of the larynx
  6. Intubation, antibiotics, tracheostomy
254
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features and treatment for vocal nodules?

A
  1. Non neoplastic nodules on the vocal cord
  2. Singers
  3. Voice abuse, smoking, alcohol
  4. single or bilateral polyps
  5. Hoarseness or change in voice
  6. Laser surgery, voice therapy
255
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features and treatment for sialadenitis?

A
  1. Salivary gland infection
  2. Bacterial uncommon
    Viral - mumps
  4. Stones can cause duct obstruction, atrophy and fibrosis of salivary glands
  5. Enlargement, redness and tenderness of glands
  6. Antibiotics if bacterial
    Fluids, massaging of glands
    Consumption of salivary stimulating foods
256
Q

What is the definition, aetiology, pathogenesis, clinical features and treatment for Ranula?

A
  1. Mucous filled cyst in the mouth
  2. Inflammation or trauma to the oral cavity
  3. Partial or total excretory duct obstruction
  4. Blueish/translucent growth on the floor of the mouth, swelling confined to the sublingual glands
  5. Aspiration and drainage
257
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features and treatment for Salivary adenoma?

A
  1. Benign tumour of salivary glands
  2. 80% in parotid gland
  3. Small proportion can become malignant
  5. Swelling near jaw/neck
    Facial numbness, muscle weakness
  6. Tend to reoccur
    Surgical removal
258
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features and treatment for oral squamous cell carcinoma?

A
  1. Cancer of the mouth
  2. 50 + males
  3. Tobacco, alcohol, UV
  4. Lower lip, tongue and floor of mouth are most common areas
  5. Ulceration, leukoplakia, erythroplakia, pain, dysphagia
  6. Surgery + radiation
259
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features and treatment for Laryngeal cancer?

A
  1. Cancer of the larynx
  2. Males 60+
  3. Smoking, alcohol, asbestos workers
  4. Unilateral lesion typically
  5. Hoarseness, leukoplakia, erythroplakia or speckled leukoplakia
  6. Radiotherapy, laser excision, laryngectomy
260
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features for eczema?

A
  1. Irritation of the skin
  2. 5% children
  3. Family history, associated with asthma + hay fever
  4. Type 1 hypersensitivity
  5. Hot, red, itchy rash, sometimes vesicles
    Chronic - leathery skin
261
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of psoriasis?

A
  1. Dermatosis characterised by regular elongation of the rate ridges
  2. 1-2% of the population
  3. Genetic and environmental
  4. Massive cell turnover, possibly autoimmune, trigger factor leading to dysfunctional immune reaction
  5. Red oval plaques on extensor surfaces - fine silvery scale
262
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of lichen planus?

A
  1. Inflammation of the skin
  2. Adults
  3. Viral hepatitis, HIV, drugs association
  4. Type 4 hypersensitivity
  5. Shiny raised purple-red blotches
    Bald patches on scalp
263
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of Lupus erythematous?

A
  1. Autoimmune disease affecting tissues of the body
  3. Discoid - skin association only
    Systemic - visceral disease +/- skin involvement
  5. Red scalp patches on sun exposed skin +/- scalp involvement
264
Q

What is the epidemiology and clinical features of dermatomyositis?

A

25% associated with underlying visceral cancer

- Heliocotropic rash + proximal muscle weakness

265
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of pemphigus?

A
  1. Autoimmune skin condition causing blisters on the skin
  3. Immunoglobulin deposition
  4. Autoantibodies directed against intercellular material
  5. Fragile blisters which rupture easily
266
Q

What is the definition and clinical features of bullous pemphigoid?

A

Sub epidermal blisters under the skin

267
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of dermatitis herpetiformis?

A
  1. Itchy blistering skin due to gluten intolerance
  2. Coeliac disease
  4. IgA deposition in dermal papillae
  5. Small itchy blisters on extensor surfaces
268
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of basal cell carcinoma?

A
  1. Commonest malignant skin tumour
  3. Sun exposure
  4. Likely to spread along nerves
  5. Nodule to ulcers
    Locally destructive
269
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of squamous cell carcinoma?

A
  1. Skin cancer
  2. Immunosuppressed at higher risk
  3. UV exposure, chronic scars and ulcers
  4. Pre cursor lesion - actinic keratosis
  5. Nodule with ulcerated crusted surface
270
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of Melanoma?

A
  1. Nodular, Lentigo maligna and acral lentiginous
  2. Lentigo - elderly
  3. P16 encoding gene mutation , BRAF gene mutation in 60%
    4.
  4. Nodular - pigmented nodule +/- ulceration highly invasive
    Lentigo - flat pigmented
    Acral lentiginous - Palms of hands, feet and under nails
271
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of systematic sclerosis?

A
  1. Multi system disease with skin and raynauds
  2. Females 30-50
  3. Exposure to vinyl chloride, silica dust
  4. Wide spread vascular damage involving small arteries
  5. Raynaud’s, beak like nose and small mouth, spider veins
272
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of Polymyalgia rheumatica?

A
  1. Muscle weakness and fatigue Large vessel vasculitis
  2. 50 + Females
  4. Unknown
  5. Stiffness in shoulders, lumbar spine and neck
    Fatigue, weight loss and fever
273
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of Muscular dystrophy?

A
  1. Muscle weakness
  2. Begins in childhood
  3. Genetic 23rd or X chromosome for protein dystrophin
  5. Progressive muscle weakness and wasting
274
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of Rhabdomyolysis?

A
  1. Destruction of skeletal muscles
  2. Mainly adults - drug users
  3. Trauma, crush injury, drugs, extreme temperature
  5. Acute renal failure - complication
    Muscle cramps, dark brown urine
275
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of osteoarthritis?

A
  1. Common joint disease - degenerative
  2. Increases with age
  3. Obesity can have a significant factor
  4. Erosion of articular cartilage
  5. Bony spurs, cysts in margins of joints
    Knees and hands in women, hips in men
276
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features and treatment of rheumatoid arthritis?

A
  1. Autoimmune inflammatory arthritis
  2. 30-50 years - females
  3. genetic factors HLA-DR4 & HLA-DRB1
  4. Synovial disease, overproduction of TNF-alpha leading to joint destruction
  5. Swollen painful and stiff joints, neuropathies, subcutaneous nodules
  6. NSAIDs, DMARDs, corticosteroids
277
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features and treatment of gout?

A
  1. Inflammatory arthritis associated with hyperuricaemia and intra articular monosodium rate crystals
  2. Common adult males
  3. Alcohol intake, diet, family history
  4. Purines broken into uric acid but excretion via kidneys is not efficient
  5. Hyperuricaemia, pain, swelling and redness in joints
  6. Weight management, anti-inflammatory meds
    Uloric and zyloprim as preventatives
278
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features and treatment of pyogenic osteomyelitis?

A
  1. Bone marrow inflammation
  2. Children
  3. Staph A and coagulase negative staph
  4. Pathogen into bone in many routes, direct inoculation, contiguous spread, haematogenous seeding
  5. Dull pain at site, fever, sweats, rigors and malaise, swelling
  6. Antimicrobial therapy
279
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features and treatment of osteoporosis?

A
  1. Skeletal disease - low bone mass and micro architectural deterioration of bone tissues
  2. Over 50s, Females
  3. Family history
  4. Increased bone breakdown
  5. Fractures
  6. Bisphosphonates
280
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features and treatment of Paget’s disease?

A
  1. Focal disorder of bone remodelling
  2. Incidence increases with age - rare under 40 - females
  3. Latent viral infection, family history
  4. Increases osteoclastic bone resorption
  5. Pelvis, lumbar spine, femur, thoracic spine, skull and tibia
    Bone and joint pain, deformities, neurological complications
  6. Bisphosphonates + NSAIDs
281
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features and treatment of Osteomalacia?

A
  1. Poor bone mineralisation due to lack of Ca2+
  2. Vitamin deficiency
  3. Hypophosphatemia due to hyperparathyroidism, vitamin D and Ca2+ deficiency
  5. Muscle weakness, waddling gait, widespread bone pain
  6. Vitamin replacement
282
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of osteosarcoma?

A
  1. Most common primary bone cancer
  2. Paget’s disease association 15-19 years
  4. Metaphysis of long bones, knees and proximal humerus
  5. Painless tumour, rapid metastasis to lung
283
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of chondrosarcoma?

A
  1. Cancer of cartilage
  2. common adult non sarcoma
    3.
  3. Pelvis, femur, humerus, scapula and ribs
  4. Dull deep pain in affected area - swollen and tender
284
Q

What is the definition, epidemiology, aetiology, pathogenesis, clinical features of Ewing’s sarcoma?

A
  1. Very rare bone cancer
  2. 15 years
    3.
  3. Mesenchymal stem cells
  4. Massive swelling commonly in long bones of arms, legs, pelvis and chest
    Weight loss, fever, paralysis, incontinence
285
Q

What is the definition, aetiology, pathogenesis, clinical features and treatment of viral warts?

A
  1. Small asymptomatic growths of skin
  2. HPV
  3. Cause proliferation and thickening of the stratum corneum, granulosum and spinousum
  4. Asymptomatic mechanical cervical cancer
  5. Topical - salicylic acid, silver nitrate, cryosurgery
286
Q

What is the definition, aetiology, pathogenesis, clinical features and treatment of pilonidal abscess?

A
  1. Cysts or abscesses in natal cleft
  2. Ingrown hair
  3. Discharge to form sinus
  4. Pain, swelling and pus
  5. Hot compress, analgesia, antibiotics, surgical excision
287
Q

What is the definition, aetiology, pathogenesis, clinical features and treatment of impetigo?

A
  1. Crusting around nares or corners of mouth
  2. Superficial skin - staph A
  4. Itchy sores that break open and leak clear fluid or pus
  5. Topical antiseptics, oral antibiotics
288
Q

What is the definition, aetiology, pathogenesis, clinical features and treatment of cellulitis?

A
  1. Infection affecting the inner layers of the skin
  2. bacterial - staph A, group A strep, B haemolytic strep
  3. Bugs enter through breaks in the skin
  4. Rubor, calor, dollar, tumour, loss of skin creases, blistering, pus exudate and fever
  5. Elevation, rest, antibiotics, pus drainage
289
Q

What is the definition, aetiology, pathogenesis, clinical features and treatment of orbital cellulitis?

A
  1. Infection of soft tissue around and behind the eye
  2. Bacterial - staph A, group A strep
  3. From skin or sinuses or haematogenous or trauma
  4. Erythema, swelling
  5. IV antibiotics
290
Q

What is the definition, aetiology, pathogenesis, clinical features and treatment of necrotising fasciitis?

A
  1. Flesh eating bacteria
  2. Type 1 - synergistic, host impairment gram negatives - obese, immune suppressed
    Type 2 - Group A strep - young
  3. 1 ischaemic tissue colonisation then infection
    2 - infection toxin release disruption in blood supply
  4. Swelling, erythema, pain, crepitus, sepsis, necrosis
  5. Surgical debridement, antibiotics
291
Q

What is the definition, aetiology, pathogenesis, clinical features and treatment of gangrene?

A
  1. Necrosis caused by inadequate blood supply
  2. Atherosclerosis, smoking, autoimmune
  3. Poor blood flow leading to tissue necrosis
  4. Dry - auto amputate
    Wet - boggy, swollen, exudate
    Gas - crepitus
  5. Surgical - source control, revascularisation, antibiotics
292
Q

What is the definition, aetiology, pathogenesis, clinical features and treatment of diabetic foot infections?

A
  2. Staph aureus, streps, corneybacterium
  3. Damage to blood vessels, ischaemia, impaired immunity and poor wound healing
  4. Holes in feet
  5. Surgical debridement, revascularisation, antibiotics
293
Q

What is the definition, aetiology, pathogenesis, clinical features and treatment of septic arthritis?

A
  1. Infection of the joint
  2. S aureus, streps, haemophilus
  3. Haematogenous spread, local spread or penetrating
  4. Pain swelling, erythema, reduced movement, sepsis
  5. Antibiotics, surgical source control - joint washout
294
Q

What is the definition, aetiology, pathogenesis, clinical features and treatment of prosthetic joint infection?

A
  1. Infection of tissue and bone
  2. Staph A, epidermidis
  3. Bugs get into surface of foreign body and immune system cannot establish biofilm
  4. Pain, instability, swelling, erythema
  5. Antibiotics, debridement
295
Q

What is the definition, aetiology, pathogenesis, clinical features and treatment of syphilis?

A
  1. STI
  2. Spirochete, treponema palladium
  3. Primary, secondary tertiary
  4. 1 - painless firm non itchy ulcer - 3-6 weeks
    2 - maculopapulae 4-10 weeks
    3 - large inflammatory swellings, gummatous, chronic gummas 3-15 years
  5. Antibiotics - penicillin
296
Q

Describe liver adenomas

A

Benign proliferation of liver cells
May be multiple
- Driven by exogenous steroids, oral contraception

297
Q

Describe adenomas of the bile duct

A

Von Meyenberg complex
Benign proliferation of bile duct cells
Tiny white nodules

298
Q

Describe Cholangiocarcinoma

A

Malignant tumour of bile duct cells
- may be due to chronic inflammation - primary sclerosis cholangitis, liver fluke
Can be central/hilar or peripheral

299
Q

Describe hepatocellular carcinoma

A

Arise in cirrhosis
Increasing incidence worldwide
Composed of malignant liver cells
Secrete AFP which can be used as a tumour marker

300
Q

What are the aetiology, risk factors, clinical features and complications of gallstones?

A

Aetiology - cholesterol, bile salts, bacterial growth and calcification
Risk - female, middle aged and overweight
Clinical Features - 80% asymptomatic
Cramy pain - biliary colic
Complications - obstruction at neck or common bile duct
- Chronic cholecystitis
- Perforation
- Obstruction at pancreatic level

301
Q

What is peutz-jeghers syndrome?

A

Autosomal dominant condition STK11 gene chromosome 19

  • Present clinically in teens or 20s with abdominal pain, GI bleeding and anaemia
  • Multiple gastric polyps
  • Mucocutaneous pigmentation
302
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of oesophagitis?

A
  1. Inflammation of the oesophagus
  2. More common in hiatus hernia
  3. Infectious and chemical
  4. Basal cell hyperplasia
  5. Ulceration, haemorrhage, perforation, Barretts oesophagus
303
Q

What are the definition, epidemiology, aetiology, barrett’s oesophagus?

A
  1. Premalignant condition with an increased risk of developing adenocarcinoma
  2. Obesity
  3. Longstanding gastro-oesophageal reflux
  4. Squamous lining replaced with columnar mucosa
  5. Longterm indigestion and heart burn
304
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of oesophageal cancer?

A
  1. Cancer of the oesophagus
  2. 8th most common cancer - more common in males, obese, caucasian
  3. Squamous cell - more common in eastern population - tobacco, HPV, thermal injury
    Adenocarcinoma - seen more in Barrett’s oesophagus
305
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of acute gastritis?

A
  1. Inflammation of the stomach lining
  3. Chemical injury - NSAIDs or alcohol
    Helicobacter pylori
  5. Effects dependent on severity - can form erosions and haemorrhage
306
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of chronic gastritis?

A
  1. Recurring gastritis
  3. Autoimmune, bacterial, chemical
  4. Risk factor for gastric neoplasia
  5. Nausea, heart burn, vomiting
307
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of peptic ulceration?

A
  1. Localised defect extending at least into submucosa
  2. Gastric - increases with age - lesser curvature of stomach, antrum
    Duodenal - increases up to 35 - more common than gastric -= bulbus
  3. Helicobacter pylori, hyperacidity, NSAIDs
  4. First part of duodenum, junction of antral body mucosa, distal oesophagus
  5. Haemorrhage, perforation, penetration into adjacent organ, stricturing
308
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of Gastric carcinoma?

A
  1. Cancer of the stomach
  2. 5th common cancer in the world
  3. Diet, H.Pylori, bile reflux, hereditary GOJ- white mass
    Body/antrum - diet association, high salt, low fruits+veg
  4. Intestinal type - Well or moderately differentiated
    Diffuse Type - poorly differentiated, scattered growth - cadherin loss/mutation
    Adenocarcinoma
  5. Pain
309
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of coeliac disease?

A
  1. Gluten sensitivity
  2. 30-60 years
  3. Immune mediated, associated with dermatitis herpetiformis - 10% of patients
  4. Reaction to gliadin, increased CD8+ intraepithelial lymphocytes
  5. Diarrhoea, abdominal pain, steatorrhoea, bloating
310
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of diverticular disease?

A
  1. Protrusions of mucosa and submucosa through the bowel wall
  2. Relationship with fibre content of diet
  3. Mesenteric and anti mesenteric Tania coli -commonly sigmoid colon
  4. Increases intra- luminal pressure
  5. 90% asymptomatic
    Cramping/abdominal pain
    Alternating constipation/diarrhoea
311
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of ulcerative colitis?

A
  1. Inflammation of colon
  2. 20-40, increased incidence in urban areas, smoking, oral contraception, X8 familial clustering
  3. Mucosal Inflammation occasionally transmural
  4. Acute - infective campylobacter, shigella, drug induced, antibiotic associated
    Chronic - idiopathic inflammatory bowel disease
  5. Diarrhoea, constipation, rectal bleeding, pain
312
Q

What are the epidemiology, aetiology, pathogenesis, clinical features and complications of crohns disease?

A
  1. 20-40, females, smokers
  2. 30-55% ileocolic
    25-35% small bowel
    15-25% colonic
    4.
  3. Chronic relapsing disease, pain, weight loss,
    Complications - toxic megacolon, perforation, fistula, short bowel
313
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of ischaemic bowel disease?

A
  1. Colonic injury secondary to an acute or chronic reduction in blood flow
  2. Vascular disease association
  3. Occlusive or non-occlusive
    3 forms
    a. Transient
    b. Chronic segmental ulcerating
    c. Acute fulminant and gangrenous
  4. Arterial embolism, arterial thrombus
  5. Cramping, abdominal pain, urge to defecate, rectal bleeding
314
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of colorectal polyps?

A
  1. Mucosa protrusion
  3. Pedunculated, sessile, neoplastic, haemartomatous, inflammatory or reactive
  4. Hyperplastic - 1-5mm found in rectum and sigmoid colon
  5. No specific symptoms
315
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of colorectal cancer?

A
  1. Cancer of the colon/rectum
  2. 2/3rd commonest cancer
    diet, obesity, alcohol, NSAIDs
  3. Familial adenomatous polyposis, Lynch syndrome
  4. Adenocarcinoma, spread - lymph
  5. Change in bowel habits, diarrhoea, constipation, PR bleeding, pain
316
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of acute pancreatitis?

A
  1. Gland reverts to normal if underlying cause is removed
  2. Alcohol
  3. Gallstones 50%, idiopathic
    Hereditary PRSS1, SPINK 1 gene
  4. Leakage and activation of pancreatic enzymes
  5. Severe abdominal pain, nausea and vomiting, raised serum amylase/lipase
    MEDICAL EMERGENCY
317
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of chronic pancreatitis?

A
  1. Irreversible loss of the pancreatic tissue - destruction of the exocrine tissue followed by destruction of the endocrine
  2. Toxic- alcohol, cigarette smoke, drugs
    Genetic - GFTR, PRSS 1, SPINK 1,
    Autoimmune
  3. Ductal obstruction
  4. Abdominal pain, weight loss, diabetes
318
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of pancreatic adenocarcinoma?

A
  2. 60-80 years, rare below 40
    smoking, family history, alcohol, nutritional and dietary factors
  3. 60-70% head of pancreas, 5-15% body, 10-15% tail
  4. Non specific symptoms
    Courvoisier’s sign - palpable gallbladder without pain
319
Q

What are the definition, epidemiology, aetiology, pathogenesis and clinical features of pancreatic neuroendocrine tumours?

A
  1. Rare pancreatic neoplasms
  2. 20-60, smoking, family history of cancer, alcohol, obesity
  3. Islet cell derived can either be malignant or benign
  4. MEN1, NF-1, VHL genes
  5. Dependent on cells in neoplasm
    Insulinoma - hypoglycaemia
    Glucagonoma - stomatitis, rash, diabetes
    Gastrinoma - peptic ulcer, diarrhoea
    Somatostatinoma - diabetes, cholelithiasis, hypochorhydria
    VIPoma - diarrhoea, hypokalaemia, achlorydria
320
Q

What are the definition, aetiology, pathogenesis and clinical features of jaundice?

A
  1. Yellowing of the skin
  2. Bilirubin >40 mol/L - commonest sign of liver disease
  3. Pre-hepatic - too much bilirubin, haemolytic anaemia - unconjugated
    Hepatic - too few functioning liver cells - mainly conjugated
    Post hepatic - bile duct obstruction by stone stricture - conjugated
  4. Yellow colour of the whites of eyes and skin
321
Q

What are the definition, aetiology, pathogenesis and clinical features of acute hepatitis?

A
  1. Liver enzymes raised - any cause, acute liver injury caused by something that goes away
  2. Damage to hepatocytes inflammatory injury, viral drugs, seronegative
  3. Toxic/metabolic injury
  4. Asymptomatic, malaise, jaundice, coagulopathy, encephalophathy, death
322
Q

What are the definition, aetiology, pathogenesis and clinical features of Chronic hepatitis?

A
  1. Liver enzymes raised Caused by something that does not go away - balance of damage and attempts repair
  2. Immunological injury - virus, autoimmune, drugs
    Fatty liver disease - alcoholic or non alcoholic
    Genetic inborn errors - iron, copper, alpha 1 antitrypsin, biliary disease, vascular disease
  3. Toxic/metabolic injury
  4. Malaise, jaundice, coagulopathy, encephalopathy, death
323
Q

What are the definition, aetiology and clinical features of viral hepatitis?

A
  1. Hepatitis A, B, C
  2. EBV, CMV, HSV usually immunocompromised host
    Same symptoms as for chronic/acute liver hepatitis
324
Q

What is the pathogenesis and clinical features of drug induced liver disease?

A

Intrinsic - every time the drug is taken - predictable
Idiosyncratic - rare, unpredictable, metabolic or immunological
Clinical features - hepatocellular damage, cholestatic, mixed liver function tests

325
Q

What are the definition, aetiology, pathogenesis and treatment of inherited haemochromatosis?

A
  1. Inborn errors of iron metabolism - bronzed diabetes
  2. Inherited haemochromatosis iron accumulation
    Liver - cirrhosis
    Skin - pigmented
    Pancreas - diabetes
    Joints - arthritis
    Heart - cardiomyopathy
    Treatment - Venesection to deplete iron stores
326
Q

What are the definition, epidemiology, aetiology, and diagnostic test and treatment of Wilsons disease?

A
  1. Inborn error of copper metabolism
  2. Younger ages
  3. Liver - cirrhosis
    Eyes - kaiser-fleischer rings
    Brain - Ataxia
  4. Test for caeruloplasmine, urine copper, plasma copper and liver biopsy
  5. Chelate copper and enhance excretion - penicillamine
327
Q

What are the definition and aetiology of alpha-1 antitrypsin deficiency?

A
  1. Abnormal anti-protease which cannot be exported from hepatocytes
  2. Alpha-1 antitrypsin deficiency
    - Anti-protease accumulated in the liver cells and injures them
    - Insufficient in blood failure to inactivate neutrophil enzymes - emphysema
328
Q

What are the definition, pathogenesis, clinical features and treatment of autoimmune liver disease?

A
  1. Autoimmune response to the liver
  2. Autoantibodies, raised IgG, ALT, other autoimmune diseases
  3. Can cause severe acute liver failure or chronic disease
  4. Immune suppression
329
Q

What are the definition, aetiology, pathogenesis and clinical features of liver cirrhosis?

A
  1. Disease affecting the liver characterised by scarring or fibrosis and conversion of the normal liver architecture into structurally abnormal nodules
  2. Fewer liver cells, end point of liver disease
  3. Pressure inside the lower increases - encircles nodules
    Liver cell failure - blood bypasses the sinusoids, reticuloendothelial cells vulnerable to infection
  4. Portal hypertension
330
Q

What are the definition, pathogenesis and clinical features of hepatic failure ?

A
  1. Acute - rare severe rapid liver injury
    Chronic - end stage of chronic liver disease
  2. Portal hypertension, structural changes, liver cell failure
  3. Chronic
    Ascites
    Muscle wasting
    Bruising
    Gynaecomastia
    Spider nave
    Varices
331
Q

What is primary biliary cholangitis - PBC?

A
  • Anti-mitochondrial antibodies
  • Elevated alkaline phosphatase
  • Bile duct granulomas at early stage
  • Ductopenia and cirrhosis
332
Q

What is primary sclerosis cholangitis?

A
  • Associated with ulcerative colitis - high alk phosphate
  • Pruned tree on biliary imaging
  • Periductal onion skin fibrosis
  • Ductopenia and cirrhosis
333
Q

What are the sterile and non sterile sites?

A

Sterile - peritoneal space, pancreas, gall bladder, liver

Non-Sterile - Mouth, oesophagus, stomach, small and large bowel

334
Q

Give a brief description of Angular cheilitis, oral herpes simplex and oral hairy leukoplakia

A

Angular Cheilitis - mild infection of the corner of the mouth caused by S.aureus or candida treated with topical anti fungals
Oral HSV - cold sores mainly via HSV-1
Oral Hairy Leukoplakia -white lesions on the tongue commonly only seen in HIV, caused by EBV

335
Q

Give a brief description of Periodontal infection, peritonsillar abscess and parotitis

A

Periodontal infection - infection of the soft tissue surrounding the teeth, can be mild (gingivitis), moderate (periodontitis) and severe (necrotising gingivitis)
Peritonsillar Abscess - quinsy, normally caused by streptococcus progenes
Parotitis - caused by staph aureus, swelling from cheek to jaw angle which can cause bacteraemia

336
Q

Give a brief description of Mucositis and helicobacter pylori

A

Mucositis - inflammation of the mucous membrane of the GI tract after chemotherapy - can cause streptococcal bacteraemia
Helicobacter Pylori - infects the gastric/duodenal mucosa causing GI symptoms +/- perforation - treatment = triple antibiotic therapy + PPI for 7-14 days

337
Q

Give a brief description of Cholangitis, cholecystitis and liver abscesses

A

Cholangitis - Infection of the biliary tree mainly caused by coliforms
Cholecystitis - infection of the gallbladder mainly caused by coliforms
Liver Abscess - bacteria from the colon - streptococcus, anaerobes and coliforms ascend into the liver and cause an abscess - treated with prolonged antibiotics and surgical drainage

338
Q

Describe the metabolic changes after trauma

A

Phase 1 - Shock
- Within 4 hours of trauma
- Blood loss, poor blood flow, low oxygen supply
Phase 2 - Hypercatabolism 24-48 hours after trauma
- Increase in basal metabolic rate
- Anaerobic metabolism
- Excessive metabolic breakdown of fat and protein
- Cytokine storm increases muscle breakdown
Phase 3 - anabolic phase 3-8 days after trauma
- Macromolecule synthesis
- Onset of recovery
- Improved appetite

339
Q

What is refeeding syndrome?

A

Fatal shifts in fluids and electrolytes that may occur in malnourished patients receiving artificial refeeding
- Moitoring of electrolytes during artificial feeding

340
Q

Describe wernicke-korsakoff syndrome

A
  • Thiamine B1 deficiency
  • Co factor form transketolase, RDH, alpha-KGDH
  • Results in mitochondrial damage, cellular necrosis, oxidative stress
  • Confusion, encephalopathy
341
Q

What are the routine LFTs?

A 
Alkaline phosphatase -ALP
ALT - alanine aminotransferase 
Bilirubin 
Albumin 
Total protein 
GGT - gamma glutamyl transferase
342
Q

What are the biochemical markers of fibrosis?

A

ELF score
PIINP
TIMP-1
Hyaluronic acid

343
Q

What are the blood tests for jaundice?

A

AST/ALT elevated and normal ALP - 90% have hepatitis

AST/ALT normal and elevated ALP - 90% have obstructive jaundice

344
Q

Describe direct and indirect pancreatic function tests

A

Direct - Invasive
- Intubation to collect aspirates in the duodenum
- Sectetin, CCK, Lundh tests
Indirect - non-invasive
- Pancreatic enzyme analysis in stools elastase
- Trypsinogen measured in blood in CF screening
- Pancreolauryl and NBT-PBA tests

345
Q

What is the clinical history, aetiology, diagnosis and antimicrobial management of salmonella gastroenteritis?

A
  1. Cramps, diarrhoea, fever, myalgia, nausea, vomiting
  2. S.Enteridis - from poultry, birds and some reptiles
    High infective dose
  3. 6-8 hours after eating
    XLD agar
  4. Ciprofloxacin 500mg twice a day for one day
346
Q

What is the clinical history, aetiology, diagnosis and antimicrobial management of shigella gastroenteritis?

A
  1. Watery, bloody, mucoid stool, abdominal pain, fluid and electrolyte loss
  2. S. dysenteries, S. flexneri, S. sonnei - from guts of humans, primates and faecal oral route
    Low infective dose
  3. 36-72 hours incubation
    DCA
  4. Ciprofloxacin 500mg twice a day for 1 day
347
Q

What is the clinical history, aetiology, diagnosis and antimicrobial management of campylobacter gastroenteritis?

A
  1. Watery diarrhoea, nausea, vomiting, malaise
  2. Heat labile toxin, poultry, birds, faecal oral route
  3. Isolate on charcoal agar
    2-5 days incubation
  4. Erythromycin 250mg-500mg four times a day for 5-7 days
348
Q

What is the clinical history, aetiology, diagnosis and antimicrobial management of Ecoli 0157?

A
  1. Watery diarrhoea then bloody diarrhoea
  2. Shiga toxin, cattle and meat
  3. MAC agar
    2-5 days incubation
  4. Do not prescribe antibiotics and avoid anti motility drugs
349
Q

What is the clinical history, aetiology, diagnosis and antimicrobial management of Clostridiodes?

A
  1. Foul smelling, watery diarrhoea, cramps, low grade fever
  2. Toxin mediated inflammation, spores aid transmission, antibiotic associated
  3. Demonstrating toxin and organism
  4. Stop predisposing antibiotic and prescribe vancomycin
350
Q

What are the 4 common viral gastroenteritis’s and their incubation periods?

A

Rotavirus - 5-7 days - children
Adenovirus - 5-7 days
Norvovirus - 1-2 days
Astrovirus - 2-3 days - children

Year 2 Medicine Leeds (4 decks)

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