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Science to Clinical Practice 1 > Inflammation > Flashcards

Inflammation Flashcards

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Biology 101 flashcards
1
Q

What is viral load in HIV?

A

Number of viral RNA genomes /ml blood

Determined by RT-PCR - reverse transcription-linked polymerase chain reaction

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2
Q

How can you diagnose HIV?

A

Presence anti-p24 (Capsid) antibodies via ELISA
Only detects individual seroconverted, 3 months after infection
Positive samples re tested mit diff ELISA/Western Blot

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3
Q

What test can detect HIV before the individual has seroconverted?

A

RT-PCR

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4
Q

What is the common treatment for HIV?

A

Highly Active Anti-Retroviral Therapy (HAART)
2 x Nucleoside Reverse Transcriptase Inhibitor (NRTI)
PLUS
1 x Non Nucleoside Reverse Transcriptase Inhibitor (NNRTI)
OR
1 x Protease Inhibitor

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5
Q

What joints are affected first in osteoarthritis?

A

Weight-bearing joints e.g. knees and hips

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6
Q

What defines a retrovirus?

A

Reverse transcription, copying RNA template (viral genome) ==> double-stranded DNA copy
Integration: covalent insertion of viral cDNA into genome of infected cell, forms provirus

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7
Q

What 3 types of polyproteins do retroviruses synthesise?

A

Gag: group specific antigen
Pol: polymerase
Env: envelope glycoprotein

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8
Q

What are some examples of the polyproteins retroviruses synthesise?

A

Gag: viral core proteins, MA (matrix), CA (capsid), NC (nucleocapsid)
Pol: PR (protease), RT (reverse transcriptase), IN (integrase)
Env: SU (surface), TM (transmembrane)

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9
Q

What are the 2 ways a retrovirus can enter a cell?

A

Receptor mediated endocytosis

Direct fusion of lipid bilayers (e.g. HIV)

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10
Q

How long does retrovirus life cycle take under permissive conditions?

A

24 hours

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11
Q

What is the negative effect of HIV reverse transcriptase having no proofreading activity?

A

Contributes to immune escape + drug resistance

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12
Q

What are some example of drugs to treat HIV that are entry inhibitors?

A

CCR5 inhibitor

Fusion inhibitor

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13
Q

What are the 2 classes of reverse transcriptase inhibitors for treatment of HIV?

A

Nucleoside-analogue reverse transcriptase inhibitors (NRTI) - incorporate ==> elongating DNA chain, X 3’OH leads to chain termination
Non-nucleotide Reverse transcriptase inhibitors (NNRTI). Allosteric RT inhibitors, X bind active site
Block initiation of RT

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14
Q

What drug affects integrase in the treatment of HIV?

A

Raltegravir, binds active site of Integrase, blocks strand transfer reaction

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15
Q

How do protease inhibitors work to treat HIV?

A

Inhibit HIV protease specifically, prevent cleavage of Gag + Gag-Pol to mature proteins
New virus particle non-infectious

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16
Q

What genetic predispositions can an individual have to get rheumatoid arthritis?

A

Human Leukocyte Antigen - HLA-DR1 + HLA-DR4

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17
Q

What is citrullination? How is it a part of rheumatoid arthritis?

A

Type II collagen + Vimentin modified
Arginine ==> Citrulline
Susceptibility genes (HLAs) mean immune system no longer recognises proteins as self and attacks

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18
Q

What is Charcot’s triad? What condition does it represent?

A

Jaundice, pain in URQ, rigors

Ascending cholangitis

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19
Q

What is Courvoisier’s law in regards to jaundice?

A

In presence of jaundice, if gall bladder palpable and non tender, jaundice unlikely due to stones
consider malignancy - pancreatic/gallbladder cancer

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20
Q

What illnesses are common in these countries?

a) Africa
b) Asia
c) SE Asia

A

a) Malaria
b) Typhoid
c) Dengue virus

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21
Q

What are key parts of the patients travel history should you keep in mind?

A

When travelled - incubation periods (time from exposure to symptoms)
What they did - business/posh hotels less risk compared to backpacking

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22
Q

What are the features of severe falciparum malaria?

A 
confusion/fits
acute renal failure
respiratory failure
hypoglycaemia
acidosis
hyperparasitaemia
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23
Q

What would you use to treat falciparum malaria?

A

IV artesunate (or quinine if artesunate x available)

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24
Q

How would you treat viral pharyngitis?

A

Symptomatic management e.g. analgesia

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25
Q

How would you treat pneumocystis jirovecii (PCP)?

A

Co-trimoxazole
Corticosteroids (prednisolone)
Oxygen therapy

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26
Q

Definition of healthcare associated infection?

A

Occurring cos of healthcare activity, not incubating at time of initial healthcare exposure
Cut off usually 48-72 hours

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27
Q

What different shapes can bacteria be identified by?

A

Coccus - round
Bacillus - rod shaped
Coccobacilli - oval shaped

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28
Q

What colour are these types of bacteria when stained?

a) Gram +ve
b) Gram -ve

A

a) Purple-blue

b) Red

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29
Q

What type of toxins do these bacteria produce?

a) Gram +ve
b) Gram -ve

A

a) Exotoxins, have teichoic acid in cell wall

b) Endotoxins in cell wall

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30
Q

What type of bacteria survives well on drying?

A

Gram +ve

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31
Q

What type of bacteria produces spores?

A

Gram +ve - some of them, not all

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32
Q 
What are the class one antibiotics?
What are the class 2 antibiotics?
A

Beta lactams, Aminoglycosides, Macrolides

Tetracyclines, Fluoroquinolones, Glycopeptides

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33
Q

What is the common gram positive cocci in clusters?

A

Staphylococcus aureus

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34
Q

What organism is the most common cause of septic arthritis?

A

Staphylococcus aureus

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35
Q

What is the common gram positive cocci in pairs and chains?

A

Streptococci

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36
Q

What are the two common gram -ve cocci?

A

Neisseria meningitidis

Neisseria gonorrhoeae

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37
Q

What is the eclipse phase in viral infections?

A

Period from virus entry until new infectious virons released

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38
Q

Definition of prodrome in viral infections

A

Non-specific symptoms appearing before more specific features (usually rash)

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39
Q

Definition of Reproductive Number (R0) in viral infections

A

Average no of secondary cases arising from a single index case in a totally susceptible population

40
Q

When would you use an oral glucose tolerance test?

A

During pregnancy for gestational diabetes

Diabetes hasn’t been around long enough to affect Hb1aC

41
Q

What are some microvascular complications of diabetes?

A

Retinopathy
Nephropathy
Neuropathy

42
Q

What are some macrovascular complications of diabetes?

A

Cerebro-vascular disease
Ischaemic heart disease
Peripheral Vascular
Diabetic foot

43
Q

What type of diabetes is ketosis prone?

A

Type 1

44
Q

How is diabetes diagnosed?

A

Symptoms of hyperglycaemia
↑ blood glc conc/HbA1c
Venous plasma glucose ≥ 11.1 mmol/l
HbA1c ≥ 48 mmol/mol

45
Q

How is diabetes diagnosed in asymptomatic patients?

A

On 2 separate occasions any of:
HbA1c ≥ 48 mmol/mol (≥6.5%)
Fasting venous plasma glucose ≥7 mmol/l
Random or 2h post 75 g glucose load ≥11.1 mmol/l

46
Q

How is prediabetes diagnosed?

A

HbA1c 43 – 47 mmol/mol (6.1-6.4%)

fasting venous plasma glc - 6.1 - 6.9 mmol/l

47
Q

Why would you not use a glucometer (capillary) to diagnose diabetes?

A

Venous plasma more accurate

Need to make sure of diagnosis

48
Q

What ketones produced lead to metabolic acidosis on DKA?

A

acetoacetate
3 hydroxy-butyrate
Organic acids

49
Q

Why are potassium levels affected in DKA?

A

Insulin causes K+ to move into cells
Without it, high extracellular K+, hyperkalaemia
Renal K+ loss, whole body K+ depletion

50
Q

What antibody complexes are formed in RA?

A

IgG and IgM

51
Q

Difference between osteoclast and osteoblast?

A

Osteoclast - breakdown of bone

Osteoblast - formation of bone

52
Q

What do the pro-inflammatory mediators in RA do?

A

Promote tissue remodelling + damage

Stimulate macrophages, fibroblasts, osteoclasts, neutrophils

53
Q

What genetic predisposition can make you more susceptible to develop RA?

A

HLA-DR1
HLA-DR4
QKRAA

54
Q

What would you see on imaging in osteoarthritis (mnemonic)?

A

L - loss of joint space
O - osteophytes
S - subchondral sclerosis
S - subchondral cysts

55
Q

What would you see on imaging in RA (mnemonic)?

A

L - loss of joint space
E - erosions
S - soft bone (osteopenia)
S - soft tissue swelling

56
Q

What condition does smoking actually reduce the risk of?

A

Ulcerative colitis

57
Q

What are the different classifications of ulcerative colitis depending on what parts of the colon are affected?

A

Proctitis - only rectum
Left-sided colitis - rectum + descending colon
Pancolitis - all of colon

58
Q

What antigens are the primary target of the immune system on a transplanted organ?

A

HLA antigens

59
Q

What type of organ donors are there?

A

Donation after brain death
Donation after circulatory death
Living donor
Expanded Criteria (EC) donor

60
Q

When can anti-HLA antibodies develop?

A

After exposure to blood products, pregnancies, prior transplants

61
Q

Where are the different classes of HLA antigens presented?

A

Class I - all nucleated cells

Class II - on APC (B cell, monocytes, dendritic cells), activated endothelial cells

62
Q

What are the 3 types of HLA antibodies?

A

A, B, DR

63
Q

When may a patient have pre-formed anti-HLA antibodies?

A

Pregnancy, Blood transfusions, Previous transplant

64
Q

What 4 key principles aid in donor-recipient matching in kidney transplantations?

A

ABO compatibility
Best HLA match (DR>B>A)
No pre-formed anti-donor HLA antibodies
Minimise cold ischaemia time

65
Q

When may A2 kidney donors be transplanted into O or B recipients?

A

If anti-A antibody titres are low (<1:8)

66
Q

What test result is an absolute contraindication for renal transplantation?

A

Positive CDC T-cell crossmatch

67
Q

When is risk of acute rejection and graft loss highest during kidney transplantation?

A

1st 3 months

68
Q

How do NSAIDs increase the risk of peptic ulcers?

A

Inhibit COX-1, reducing prostaglandin production - cytoprotective

69
Q

How does the Helicobacter pylori bacteria cause peptic ulcers?

A

Burrow into mucosa, allowing acid to reach other layers

70
Q

Why may amylase levels be normal if taken 24-48 hours later in a patient with pancreatitis?

A

Excreted by kidneys

71
Q

What obstructions can cause appendicitis?

A 
Inflamm of vermiform appendix
Faecolith
Stool
Infective agents
Lymphoid hyperplasia
72
Q

What is the common bacteria in appendicitis?

A

Bacteroides fragilis + E coli

73
Q

What type of T helper response is prominent in:

a) U.C?
b) Crohn’s?

A

a) Th2

b) Th1

74
Q

What does a stool MC&S test in U.C and Crohn’s exclude?

A

Campylobacter, C.diff, Salmonella, Shigella, E.Coli, Amoeba

75
Q

What are the 3 features of renal bone disease/CKD -MBD?

A

Osteomalacia - softening of bones
Osteoporosis - brittle bones
Osteosclerosis - hardening of bones

76
Q

What is the most common cause of nephrotic syndrome in:

a) Children?
b) Adults?

A

a) Minimal Change disease

b) Focal Segmental glomerulosclerosis

77
Q

What is the most common cause of primary glomerulonephritis?

A

IgA nephropathy AKA Berger’s disease

78
Q

What is an:

a) Uncomplicated UTI?
b) Complicated UTI?

A

a) Female, first presentation, not pregnant, immunocompetent

b) male, recurrent UTIs, elderly, catheter related, children, pyelonephritis

79
Q

What is pyuria?

A

Presence of WBC in urine, >10 per HPF x400

80
Q

What part of the urinary tract is involved in:

a) Upper UTIs?
b) Lower UTIs?

A

a) Kidneys and ureters

b) Bladder, Urethra, Prostate (male)

81
Q

What are some examples of:

a) Upper UTIs?
b) Lower UTIs?

A

a) Pyelonephritis, Intrarenal/perinephric abscess

b) Cystitis, Urethritis, Prostatitis

82
Q

What bacteria is the most common cause of UTIs?

Acronym for most common ones?

A

E. Coli

SEEEK PP - Saprophyticus, E.Coli, Enterococcus. Enterobacter, Klebsiella, Proteus, Pseudomonas

83
Q

What is an ascending infection in UTIs?

A

Bact move from rectal area → urethra → bladder → kidney

84
Q

What is a descending infection in UTIs?

A

Bact starts in blood/lymph → kidney → bladder → urethra

85
Q

Why is antibiotic Nitrofurantoin avoided in 3rd trimester of pregnancy in treatment of UTIs?

A

Linked with haemolytic anemia in new-born

86
Q

What arteries and veins are used to make a arteriovenous fistula?

A

Radiocephalic, Brachiocephalic, Brachiobasilic

87
Q

What enzyme converts unconjugated bilirubin to conjugated bilirubin?

A

Glucuronyl transferase enzyme

88
Q

Definition of:

a) Jaundice
b) Icterus

A

a) yellow discoloration of skin, mucous membranes and sclera due to hyperbilirubinemia
b) specific yellow discolouration of sclera due to hyperbilirubinemia, usu visible before jaundice develops elsewhere

89
Q

Why would you get gynaecomastia in alcoholic liver disease?

A

Liver breaks down oestrogen, so when it’s ill, cannot break down

90
Q

What is the difference between compensated and decompensated liver cirrhosis?

A

Compensated - liver is coping, no symptoms

Decompensated - liver x cope, symptoms

91
Q

What can be given to help patients with diabetes insipidous?

A

Desmopressin - synthetic ADH

92
Q

What 2 things increase calcium levels in body?

A 
PTH
Vit D (Calcitonin)
93
Q

What is the role of PTH?

A

Increase:
osteoclast activity in bones (reabsorbing Ca from bones)
Ca absorption from the gut
Ca absorption from the kidneys (LoH + distal tubules)
Vit D activity - turn to active form

94
Q

What is primary hyperparathyroidism?

How treat?

A

Tumor (adenoma commonly) in parathyroid gland
Hypercalcaemia, low phosphate,
Surgically remove tumour

95
Q

What is secondary hyperparathyroidism?

How treat?

A

Low Vit D intake/chronic renal failure, low Ca resorbed (hypocalcaemia) so high levels PTH
Correct Vit D insufficiency/renal transplant

96
Q

What is tertiary hyperparathyroidism?

How treat?

A

After prolonged secondary hyperparathyroidism, hyperplasia of glands
When secondary treated. PTH still high so hypercalcaemia
Surgically remove PT gland so PTH normal

97
Q

What is primary hypoparathyroidism?

How treat?

A

decreased PTH gland failure/parathyroid surgery
low Ca, high phosphate
Ca supplement (alfacalcidol)

Science to Clinical Practice 1 (5 decks)

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