Commonly Forgotten set 2 Flashcards
(89 cards)
1
Q
What is the most common cause of infective endocarditis?
A
Strep. Viridans MOST COMMON other enterococci (Staph aureus/epidermis, strep Bovis, H Influenzae)
2
Q
list 7 key ie features
A
Splinter haemorrhages Osler’s nodes Janeway lesions Roth’s spots Fever New murmur septic Emboli
3
Q
How is DUKE’s diagnosis for Infective endocarditis used?
A
(DUKE’s need 2 major, 1 minor to diagnose OR 1 major and 3 minors)
Major
+ve blood culture (2 separate cultures or persistently +ve e.g. 3> 12 hours apart)
Endocardium involved as shown by +ve echo → vegetation, abscess, OR new valvular regurgitation
Minor
Predisposing (cardiac lesion/IVDU)
Fever >38 degrees
Valvular/immunological signs
+ve blood culture that doesn’t meet major criteria
+ve ECHO that doesn’t meet major criteria
4
Q
What is typical infective endocarditis treatment?
A
(IV) (Amoxicillin + gentamicin)
5
Q
Name most common CAP and HAP
A
CAP S.pneumoniae
HAP P. Aeruginosa
6
Q
CAP and HAP treatments
A
CAP Antibiotics – amoxicillin (if severe co-amoxiclav) + Clarithromycin
HAP Antibiotics – If MRSA then use Vancomycin
7
Q
Osteomyelitis initial treatment
A
ceftriaxone
8
Q
Describe LP in Bacterial Meningitis
A
Low glucose, high protein, cloudy, polymorph white cells = Bacterial meningitis
9
Q
Describe LP in viral Meningitis
A
Higher glucose, low protein, clear, mononuclear white cells = Viral meningitis
10
Q
Lower UTI antibiotic
A
Trimethoprim
11
Q
Upper UTI antibiotic
A
Ceftriaxone +- cefuroxime
12
Q
Complicated malaria treatment
A
Artesunate or Quinine (both IV)
13
Q
Uncomplicated malaria treatment
A
PO Riamet
14
Q
Drug for Hypnozoite clearance
A
Primaquine
15
Q
HIV test?
A
ELISA
16
Q
HIV Treatment scheme?
A
HAART
17
Q
Types of Necrotising Fasciitis
A
Type 1: POLYMICROBIAL → mixture of anaerobic (clostridium perfrigens) + aerobic bacteria
Type 2: Single bacteria (esp. group A strep)
18
Q
Necrotising Fasciitis treatment
A
Empirical Abx’s: IV benzylpenicillin + clindamycin
19
Q
Cellulitis treatment
A
Penicillin V (phenoxymethylpenicillin) + Flucloxacillin
20
Q
Impetigo treatment
A
Topical or systemic antibiotics, erythromycin, or if allergic/MRSA doxycycline, clindamycin
21
Q
Impetigo presentation
A
Fluid filled blisters (bullous), local swollen lymph nodes
22
Q
What is the main infective agent in cellulitis?
A
Group A beta haemolytic streptococci: strep pyogenes
23
Q
Describe gram staining process
A
Apply a primary stain such as crystal violet (purple) to heat fixed bacteria
Add iodide which binds to crystal violet and helps fix it to the cell wall
Decolorize with ethanol or acetone
Counterstain with safranin (pink)
24
Q
Name some Gram positive Cocci
A
Staph, strep, entero
25
Name some Gram positive bacilli
Corynebacteria
Clostridia
Bacillus
26
Name some Gram negative Cocci
Neisseria
| Moraxella
27
Name some Gram negative bacilli
```
E coli
Campylobacter
Pseudomonas
Salmonella
Shigella
Proteus
```
28
name a G+ve, Streptococcus which is Beta haemolytic and lancefield group A
Strep. Pyogenes
29
name a G+ve, aerobic Streptococcus which is Beta haemolytic and lancefield group B
Strep. agalactiae
30
name a G+ve, aerobic Streptococcus which is Alpha haemolytic
Strep. pneumoniae
Strep. Oralis
Strep. milleri
Strep. sanguis
31
name a G+ve, aerobic Streptococcus which is non-haemolytic
```
Strep Bovis
Enterococcus faecalis (lancefield D)
```
32
Name a G+ve, aerobic staphylococcus which is coagulase/DNAse positive
Staph. aureus
33
Name a G+ve, aerobic staphylococcus which is coagulase/DNAse negative
all staph apart from staph. aureus
34
Name a G -ve, lactose fermenting bacillus
Coliforms
Escherichia coli
Klebsiella pneumoniae
35
Name a G -ve, non-lactose fermenting bacillus which is oxidase positive
Pseudomonas aeruginosa
36
Name a G -ve, non-lactose fermenting bacillus which is oxidase Negative
Enterobacteriaceae:
Shigella
Salmonella
Proteus
37
Name an optochin sensitive aerobic alpha haemolytic gram positive coccus
Streptococcus pneumoniae
38
Barrett's Oesophagus
Metaplasia from squamous to columnar
39
Stages of wound healing
Clotting phase
Healing of a wound begins with clot formation to stop bleeding and to reduce infection by bacteria, viruses and fungi. Clotting is followed by neutrophil invasion.
Inflammation phase
In the inflammatory phase, macrophages and other phagocytic cells kill bacteria.
Proliferative phase
In the proliferative phase, immature granulation tissue containing plump, active fibroblasts forms
Maturation phase
During the maturation phase of wound healing, unnecessary vessels formed in granulation tissue are removed by apoptosis, and type III collagen is largely replaced by type I.
40
Stages of healing from inflammation damage
Recall phase
In the recall phase the adrenal glands increase production of cortisol which shuts down inflammation.
Resolution phase
In the Resolution phase, pathogens and damaged tissue are removed by macrophages (white blood cells).
Regeneration phase
In the Regeneration phase, blood vessels are repaired and new cells form in the damaged site similar to the cells that were damaged and removed.
Repair phase
In the Repair phase, new tissue is generated which requires a balance of anti-inflammatory and pro-inflammatory eicosanoids.
41
Give an example of a 5-alpha-reductase inhibitor
Finasteride
42
What might a 5-alpha-reductase inhibitor be used to treat?
BPH and hair loss
43
Give a DOAC example
Rivaroxaban
44
What system is used to assess BPH treatment?
The international prostate symptom score
45
Of what is the The international prostate symptom score comprised?
8 questions, (7 symptom and 1 QOL) assessing progress and treatment of BPH
46
A term given to an occupational lung disease caused by dust inhalation:
Pneumoconiosis
47
What systems do a schistosomiasis infection affect?
UT, bowel
48
Where is one likely to contract schistosomiasis ?
Tropical countries
49
schistosomiasis treatment
praziquantel
50
schistosomiasis significant features
```
Blood in stool
Eggs in stool
Antibody present in blood
Multi-organ failure - ascites
Seizures, rash and fever
```
51
Pathogen in Syphilis
Treponema pallidum
52
Features of Systemic Inflammatory Response Syndrome (SIRS)
Temperature >38.3oC or <36oC
Heart rate >90
White Cell count >12x10^9 per L
Hypoxia
53
What is the scoring system for peripheral vascular disease?
The Fontaine Classification (1-4)
54
Classic features of CML
```
Usually 40-60yrs age
Slow onset
Sometimes incidental finding
High WCC
Splenomegaly
Metabolic features
Philadelphia chromosome detected by BCR/ABL dual colour dual-fusion probe
```
55
CML treaatment
Imatinib
56
How is myeloma bone disease usually assessed?
Plain x-ray
Shows lytic lesions
Osteoclast-activating factors
OAFs include RANKL, IL-3 and TNF-α
57
Signs of Sarcoidosis
Raised ACE
Raised Calcium with normal PTH
Bilateral lymph node enlargement
must exclude TB
58
ECG evidence of Aortic Stenosis:
Bifid P-wave (P-mitrale)
59
Gout pain medication
Colchicine
| If intolerant, diclofenac (NSAID)
60
What is used to calculate to possibility/extent of peripheral artery disease?
ankle-brachial pressure index (<0.5 is critical, 0.5<0.9 is some arterial disease)
61
What is the treatment used for acute alcohol poisoning?
Metadoxine is used for clearance
| Thiamine is used to prevent wernicke-korsakoff syndrome
62
Name a v2 receptor antagonist
Tolvaptan
63
Describe complement:
The complement system consists of a number of small proteins found in the blood, synthesised by the liver, which circulate as inactive precursors (pro-proteins)
When stimulated by one of several triggers, proteases in the system cleave specific proteins to release cytokines and initiate an amplifying cascade of further cleavages. The end result of this complement activation or complement fixation cascade is stimulation of phagocytes to clear foreign and damaged material, inflammation to attract additional phagocytes, and activation of the cell-killing membrane attack complex.
64
Functions of complement
Complement triggers the following immune functions:[5]
1. Phagocytosis – by opsonizing antigens. C3b has most important opsonizing activity
2. Inflammation – by attracting macrophages and neutrophils
3. Membrane attack – by rupturing cell wall of bacteria
65
What does the Membrane Attack complex (MAC) do?
The membrane-attack complex (MAC) forms transmembrane channels. These channels disrupt the cell membrane of target cells, leading to cell lysis and death.
Active MAC is composed of the subunits C5b, C6, C7, C8 and several C9 molecules
66
What is the role of opsonisation?
It enhances phagocytosis by marking an antigen for an immune response or marking dead cells for recycling
67
What drug is used to treat a focal seizure?
Carbamazepine
68
What drugs are used to treat focal and generalised seizures?
Valproate
| Lamotrigine
69
What drugs are used to treat generalised seizures?
Ethosuximide (absence only)
| Rufinamide
70
What protein aggregations can be observed in the cytoplasms of AML blast cells?
Auer rods
71
Term given for the easy bruising seen in leukaemia
Petechiae
72
The term given to the treatment scheme for high - grade non-Hodgkin's lymphoma
R-CHOP Combined chemotherapy and monoclonal antibodies - kill or cure
Rituximab
Zevalin - Radioimmunotherapy
73
Diagnostic signs of Multiple Myeloma:
Rouleaux stacks - aggregated erythrocytes in blood film
High ESR
Monoclonal protein in blood and urine (Bence Jones protein)
Light chain deposition in the kidneys
Pepperpot skull
74
Clinical signs of Multiple Myeloma:
```
CRAB:
High calcium
Renal
Anaemia
Bone disease
Amyloidosis
```
75
What are the two categories of Polycythaemia?
Relative Polycythaemia: ↓Plasma volume, normal RBC Mass
| Absolute Polycythaemia: ↑RBC Mass, normal plasma volume
76
Test to characterise blood clotting (intrinsic pathway)
activated partial thromboplastin time
77
Test to characterise blood clotting (extrinsic pathway)
The prothrombin time (PT)—along with its derived measures of :
- Prothrombin ratio (PR)
- International normalised ratio (INR)
78
What are the main platelet disorders (with a primary cause)
ITP - Immune thrombocytopenia - antiplatelt Autoantibodies - low clotting
TTP - Thrombotic Thrombocytopenic Purpura - SLE - too much clotting
79
pathology of thalassaemia
Unbalanced production of Hb chains, with one being less abundant than the other. divided into 𝞪 and 𝜷 thalassaemia, for obvious reasons.
80
Parkinson's signs
```
Festinating gait
Bradykinesia
Rigidity
Tremor
off/on dyskinesia
It is assymetrical
```
81
Antibodies found in Coeliac's
Anti TTG, anti-endomysial and anti-alpha gliadin
82
What does a "tinkling" bowel sounds indicate?
Obstruction
83
What investigation is used to look for diverticulitis?
A barium enema
84
test for H pylori
the rapid urease test
85
What is a Mallory- Weiss tear?
An oesophageal tear due to coughing or vomiting or alcoholism
Urgent endoscopy
86
Cardioprptective drug before treatment of Hyperkalaemia of Hypercalcaemia
Calcium Gluconate
87
Ascending cholangitis - classic presentation:
Reynold's Pentad: right upper quadrant pain, jaundice, and fever (charcot's triad), Low blood pressure (or shock) and confusion
88
Famous wilson's disease sign
Kayser-Fleischer rings
89
Common Primary Biliary Cirrhosis signs
For cirrhosis in general: CLAPS - Clubbing, Leukonychia, Ataxia, Palamar erythema, Scratch marks
For PBC, AMA +ve, high ALP,
Xanthoma (fatty collections around eyes)
