Year 5 😊✌🏼 > Path 3 > Flashcards

Path 3 Flashcards

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1
Q

Risk factors for SSI

A
  • age (>45)
  • ASA 3 or more
  • diabetes
  • malnutrition
  • low serum albumin
  • DMARDs
  • obesity (adipose tissue is poorly vascularised)
  • smoking
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2
Q

Main pathogens causing SSI

A
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3
Q

FC levels of SSI deep superficial etc

A
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4
Q

Measures to decrease number of surgical site infections

A

PRE-OP
- pre-op showering
- nasal décolonisation (for some surgeries, e.g. cardiac)
- antibiotic prophylaxis (at induction of anaesthesia, need to achieve bactericidal levels at the time the incision is made; in prolonged OP or lots of blood loss,
- hair removal not with razor but electrical clippers because prevent micro abrasions

OP
- reduce number of poeple in theatre
- ventilation (+ve pressure, direction of air flow is from theatre to rest of the hospital; 20 air changes/h, all air coming in is filtered, keep theatre doors closed; orthodoxy surgeries in laminar flow theatres)
- sterilised instruments
- skin prep (chlorhexidine in 70% EtOH)
- asepsis and surgical technique
- normothermia
- O2 sats >95%

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5
Q

Incidence of SA

A
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6
Q

Incidence of SA

A
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7
Q

mortality and morbidity in SA

A
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8
Q

RFs for SA

A
  • prosthesis
  • immunosuppression
  • underlying joint disease
  • IVDU
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9
Q

Pathophysiology of SA

A

see screenshot

includes bacterial and host factors

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9
Q

Pathophysiology of SA

A

see screenshot

includes bacterial and host factors

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10
Q

Host factors for SA pathophysiology

A
  • genetic variation in cytokine expression
  • more
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11
Q

bacterial factors in SA pathophysiology

A
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12
Q

Commonest pathogens

A
  • staph aureus
  • streptococci
  • gram -ve organisms
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13
Q

Presentation of SA

A
  • ## 1 red, hot, swollen joint
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14
Q

Ix for SA

A
  • blood cultures
  • synovial aspiration
  • bloods

USS to guide needle aspiration
MRI scan to look at damage and

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15
Q

Abx for SA

A

flucloxacillin
cephalosporin

may need to add vancomycin if MRSA

review after 2 weeks -> switch to oral for 4w if good response, if not good continue for 4 weeks IV

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16
Q

Vertebral osteomyelitis

A
  • acute haematogenous
  • add
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17
Q

Commonest organisms in vertebral osteomyelitis

A
  • staphylococcus
  • streptococci
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18
Q

commonest location of

A

lumbar spin

  1. cervical spine
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19
Q

PC in VOM

A
  • back pain
  • fever
  • may have neurological sx
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20
Q

Ix in VOM

A

MRI?

add mroe

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21
Q

Mx of VOM

A
  • 6w Abx
  • may need longer course if untrained abscess, foreign material
  • may need surgery if there are neurological issues/compression
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22
Q

commonest organisms causing prosthetic joint infection

A
  • coagulase -ve staphylococci
  • staph aureus
  • g-ve less common
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23
Q

what dies the presence of alpha-defensin indicate?

A

infection (in the bone)

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24
what dies the presence of alpha-defensin indicate?
infection (in the bone)
25
What haematological changes are normal in pregnancy?
- mild anaemia (physiological) - plasma volume rises 150%, red cell mass rises 120-130%) - macrocytosis (normal - physiological, but does not exclude folate or b12 deficiency) - neutrophlia - thrombocytopenia (and increased platelet size)
26
iron deficiency in pregnancy - consequences
IUGR prematurity PP haemorrhage
27
Dose of folate pre conception and in first trimester
400 ug/day
28
What happens to platelets in pregnancy?
count decreases (15% women will have below 150) size increases there may also be some clumping
29
Causes of thrombocytopenia in pregnancy
- physiological - pre-ecclampsia - ITP - microangiopathic syndromes - other (e.g. DIC, leukemia, ...)
30
thrombocytopenia number
<140 x 10^8 /L double check this
31
IgG autoantibodies from ITP can cross the placenta so the baby may be affected significantly low platelets (<20) in 5% of the babies
32
How do you manage ITP in pregnancy?
- steroids ?check IViG?
33
HUS and I think there is a lot more to say here and I think there is so much more to say here
34
What medication can be given to women to increase uterine contraction?
syntosin (synthetic oxytocin)
34
What medication can be given to women to increase uterine contraction?
syntosin (synthetic oxytocin)
35
When around pregnancy is the risk of VTE highest?
6 weeks following delivery VTE risk assessment done before, throughout and after pregnancy good hydration is important during pregnancy
36
Causes of DIC
- infections - obstetric causes fill out this list
37
Scan to check for metabolically active metastases?
FDG-PET
38
Scan to check for bone metastases?
Tc bisphosphoante scan
39
What happens to the apex beat in LV hypertrophy?
the apex beat is normal LV hypertrophy does not cause apex displacement. tall R waves and deep s-waves because the muscle is huge. you only see displacement if there is also heart failure do not confuse a dilated heart with a hypertrophic heart
40
commonest cause of LV hypertrophy
untreated HTN
41
What type of bacteria are neisseria gonorrhoeae?
gram -ve diplococci
41
What type of bacteria are neisseria gonorrhoeae?
gram -ve diplococci
42
What can cause gram -ve meningitis in children? (rods)
43
g-ve diplococci on LP in meningitis Sx
Neisseria meningitidis
44
g-ve rods causing meningitis Sx in a 6yo child - organism?
Haemophilus influenzae less common in vaccinated kids but in the unvaxxed E coli is also a gram -ve rod and causes meningitis in neonates and premies
45
gram +ve diplococci causing sepsis that we are worries about
strep pneumoniae
46
19 yo with PUO cultures -ve for 2 months but cold agglutinins are positive - organism?
mycoplasma - gives you cold agglutinins ?also takes long to culture?
47
gram+ve cocci in clusters from pus of a boil
staph aureus the clusters make it likely to be staph aureus it is the aggressive organism that attacks joints, foreign material etc.
48
staph epidermidis
found on skin can also cross the skin and cause sx much less aggressive than staph aureus
49
Strep viridans
gram +ve cocci can cause strep viridans endocarditis PUO slowly can damage the endocardium
50
Which organism are you more likely to get endocarditis/sepsis from? strep pyogenes and strep viridans
strep pyogenes kills you by sepsis before it can settle on valves strep viridans can cause PUO and endocarditis because it is less virulent and can settle on the valve more virulent bugs may be less likely to cause endocarditis thereby
51
Signs of subacute endocarditis
- splenomegaly - haematuria - splinter haemorrhages - heart murmurs
52
Where does strep viridans come from
teeth
53
What is the commonest cause of meningitis
viral e.g. coxsackie B virus
54
what is aseptic meningitis?
viral meningitis
55
how do you manage viral meningitis?
?supportive management
56
LP result in SAH
- red cells - yellow colour
57
Stain in TB
Ziehl nielsen
58
LP result in TB meningitis
normal LP but culturign shows TB
59
Commonest cause of secondary immunodeficiency worldwide
malnutrition especially protein loss malnutrition
60
measles induced immunodeficiency
- lasts months to years - implicated in increased morbidity and mortality
61
How does TB lead to immunodeficiency?
???
62
TB IRIS
TB immune reconstitution syndrome
63
Drugs as a cause of immunodefiocicnet
1. small molecules (steroids, cytotoxic agents, calcineurin inhibitors, anti epileptic drugs, DMARDs) 2. Jak inhibitors 3. biologics and cellular therapies 4. haematological cancers (B-cell and plasma cell cancers; chemotherapy; Goods' syndrome)
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Goods' syndrome
- thymoma associated with Ab deficiency - combined T- and B-cell problem - absent B cells, no antibodies - increased risk of PJP, CMV, fungal and AI disease
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Ix for ?secondary ID
FISH FBC Immunglobulins S?? HIV test
65
Ix for ?secondary ID
FISH FBC Immunglobulins S?? HIV test
66
How many people are living with HIV?
37 million
67
How many of the people living with HIV are taking ART
21 million of 47 million
68
How many poeple in the UK are living with HIV?
101 200 approx 100 000
69
virus family of HIV
lentivirus family
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what kind of virus is HIV?
double stranded RNA virus structural, replicative and accessory proteins retrovirus
71
What does HIV bind to?
CD4 CCR5 CXCR4
72
How does HIV replicate?
via DNA intermediate integrates into host genome HIV DNA transcribed to viral mRNA viral RNA translated to viral proteins packaging and release of mature virus
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Origin of HIV
4 distinct linneages MNOP
74
commonest variant of HIV worldwide
Group M
75
natural history of HIV infection
1. acute (flu-like illness in 70% people) 2. asymptomatic but progressive for 8-10 years 3. AIDS
76
what is the risk of HIV transmission related to?
viral load therefore risk of transmission is highest in the acute phase
77
driving force for viral diversity in HIV
error prone nature of HIV RT short generation time of viral cycle and length of infection
78
Characteristic features of untreated HIV imunlogy
insert
79
loss of tetanus vaccine responses in HIV
80
ART in UK
-reverse transcriptase inhibitor (NRTI, NNRTI) - boosted protease inhibitors (ritonavir + PI) - integrates inhibitor ( ........
81
who is typically affected by MDS?
elderly
82
signs and sx of myelodysplasia
of general BM failure
83
Issues in MDS
1. cytopenias 2. quality decline of the cells 3. increased risk of AML
84
Pelger Heut abnormallity
bi-lobed neutrophils seen in MDS
85
Blood and BM morphological features of MDS
- Pelger Huet abnomrality - dysgrabnulopoiesis of neutrophils - dyseryhtropoiesis of erythrocytes - myelokathexis - ringed sideroblasts - myeloblasts with Auer rods (seen in AML) ..... more
86
what do Auer rods indicate?
AML
87
Scoring system for MDS
IPSS-R revised international prognostic scoring system the higher the score the higher the lower the survival and time to progress to AML
87
Scoring system for MDS
IPSS-R revised international prognostic scoring system the higher the score the higher the lower the survival and time to progress to AML
88
MDS genetic abnormalities
- driver mutations in MDS (carry prognostic significance) add more info
89
Myelodysplasia - Evolution
1. deterioration of blood counts (worsening consequences of marrow failure) 2. development of AML (in 5-50% <1 year, some cases of MDS are much slower to evolve, AML from MDS has an extremely poor prognosis and is usually not curable 3. 1/3 will die of infection 1/3 will die of bleeding 1/3 will die of acute leukaemia
90
Treatment of MDs
1. allogenic SCT 2. intensive chemotherapy only a minority of MDS patents can really benefit from this
91
Supportive care in MDS
1. Supportive care - blood transfusion - antimicrobial therapy growth factors (Epo, G-CSF, TPO-receptor agonist) 2. Biological modifiers - immunosuppressive therapy - azacytidine - decitabine - lenalidomide 3. oral chemotherapy hydroxyurea/ hydroxycarbamide 4. low dose chemotherapy )s.c. low dose cytarabine) 5. intensive chemo/sct in a minority of patients
92
when do you use lenalidomide
MM 5qdel variant of MDS
93
Primary causes of BM failure
94
Secondary causes of BM failure
95
What is more common - primary or secondary BM failure?
secondary is much more common
96
Drugs and BM failure
1. predictable (dose dependat, common) - cytotoxic drugs 2. idiosyncratic (NOT dose dependant, rare 3. Antibiotics etc/
97
What is chloramphenicol used for?
it is used as an antibiotic in eye drops used to be a systemic medication; can cause BM failure
98
incidence of aplastic anaemia?
2-5 cases/million/year slightly more common in Asian pop
99
Which age groups are affected by aplastic anaemia
all age groups can be affceted bimodal incidence in 20s and 60s
100
Causes of aplastic anaemia
70-80% are idiopathic inherited: dyskeratosis congenita, Fanconi anaemia, Schwachmann-diamond syndrome secondary anaemia: radiation, drugs, viruses, immune e.g. SLE miscellaneous: PNH (paroxysmal nocturnal haemoglobinuria), thymoma
101
idiopathic aplastic anaemia
failure of BM to produce blood cells stem cell problem (CD34, LTC-IC immune attack
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triad of BM failure
1. anaemia (fatigue, breathlessness) 2. leucopenia (infections) 3. thrombocytopenia (bruising)
103
diagnosis of MDS
1. blood (cytopenia) 2. marrow (hyopcellular)
104
Ddx of pancytopenia and hypo cellular marrow
- hypoplastic MDS / AML - hypocellular ALL - hairy cell leukemia - mycobacterial (usually atypical infection) - anorexia nervosa - idiopathic thrombocytopenic purpura (BM tap will be normal)
105
Camitta criteria
low reticulocyte count low neutrophils low platelets BM <25% cellularity`
106
Mx of BM failure
1. seek and remove cause (detailed drug and occupational hx) 2. supportive (blood transfusion, abx, iron chelation therapy) 3. Immunosuppressive therapy (anti-thymocyte globulin, steroids, CyA) 4. drugs to promote marrow recovery (G-CSF, TPO R agonists, oxymethome) 5. SCT 6. other treatments in refractory cases e.g. aletuzumab (anti-CD52, high dose cyclophosphamide)
107
Specific treatment of idiopathic aplastic anaemia is based on...
- illness severity - age of patient - potential stem cell donor
108
Specific treatment of idiopathic aplastic anaemia
insert
109
late complications following immunosuppressive therapy for AA
1. relapse of AA (35% over 3 years) etc small risk fo solid tumours
110
cure rate of young patients with AA treated with SCT
80%
110
cure rate of young patients with AA treated with SCT
80%
111
Fanconi anaemia
most common form of inherited AA AR x-linked inheritace etc
112
Fanconi anaemia
most common form of inherited AA AR x-linked inheritace etc
113
What is the most common cause of inheritedAA?
Fanconi anaemia
114
somatic/congential abnormalities in Fanconi anaemia
short stature cafe au lait spots abnormality of thumbs developmental delay hypo pigmented patches skeletal abnormality check and add details
115
complications of fanconis anaemia
AA (90%) median age 9 leukemia 10% - 14 liver disease cancer\ ????
116
dyskeratosis congenita
inherited d/o characterised by - BM failure - cancer predisposition - somatic abnormalities nail dystrophies leukoplakia white patches n skin rare!! add more details
117
dyskeratosis congenita
inherited d/o characterised by - BM failure - cancer predisposition - somatic abnormalities nail dystrophies leukoplakia white patches n skin rare!! add more details
118
DC genetic basis
telomere shortening X-linked, AD or AR possible DKC1 gene and TERC gene
119
which genes are implicated in DC (dyskeratosis congenita)?
120
telomere shortening is a feature of idiopathic aplastic anaemia and also of dyskeratosis congenital
121
mx options for hypoglycaemia
Alert and orientated - juice/sweets - sandwish drowsy/confused but swallow intact - buccal glucose - hypostop/glucofgel - start thinking about IV access unconscious or concerned about swallow -IV access - 20% glucose ... im iv etc
122
Sx of hypoglycaemia
1. adrenergic - tremor - palpitations - sweating - hunger 2. neuroglycopaenic - somnolescnece - confusion - incoordination - seizures, coma 3. None = impaired awareness of hypoglycaemia (could be people that take insulin) relief of sx with glucose administration
122
Sx of hypoglycaemia
1. adrenergic - tremor - palpitations - sweating - hunger 2. neuroglycopaenic - somnolescnece - confusion - incoordination - seizures, coma 3. None = impaired awareness of hypoglycaemia (could be people that take insulin) relief of sx with glucose administration
123
Counter-regulation in hypoglycaemia
low glucose -> decrease in insulin, increase in glucagon 1. reduces peripheral uptake of glucose 2. increases glycogenolysis 3. increases gluconeogenesis 4. increases lipolysis increased lipolysis increases FFAs -> become ATP via beta oxidation; a by-product of this is ketone body production the minute you have insulin you will have no lipolysis Low neuronal glucose is sensed in the hypothalamus and leads to 1. sympathetic activation - catecholamines 2. ACTH, cortisol, GH
124
Ix in hypoglycaemia
- confirm that there is hypoglycaemia with glucometer - may be more difficult in person that is otherwise healthy because it might be difficult to get a sample at the time they are hypo whereas people with diabetes monitor their blood glucose regularly
125
venous vs capillary BG measurement
capillary - poor precision and low levels of glucose if you think there is hypoglycaemia the gold standard is lab measured venous glucose
126
Reasons why people without diabetes develop hypoglycaemia
- post gastric bypass - organs failure - extreme weight loss - factitious - hyperinsulinism - critically unwell fasting or active paediatric vs adult
127
What to consider in hypoglycaemia in people with diabetes?
medications inadequate CHO intake / missed meals impaired awareness excessive alcohol strenuous exercise co-existing AI conditions (e.g. exclude Addisons)
128
Which meds can cause hypglyxameia
glucose lowering drugs (sulphonylureas, meglitinides, GLP-1 agents) Insulin (rapid acting with meals, inadequate meal. long acting at nighty or in between meals) Other drugs (b-blockers, salicylates...) add
129
Impaired awareness of hypoglycaemia
insert
130
Ix for hypoglycaemia in someone w/o diabetes?
- thorough hx and examination biochemical tests (do them at the right time) - insulin levels * - c-peptide* - drug screen* (e.g. sulfonylurea) - auto-antibodies - cortisol/GH - FFA/blood ketones* - lactate * indicates the most basic tests. you would not do an autoantibody screen on everyone
131
Why do we measure both insulin and c-peptide in hypoglycaemia
because c-peptide is a marker for endogenous insulin. endogenous and exogenous insulin contribute to the insulin level but only endogenous contributes to c-peptide level
132
hypoglycaemia with high insulin, low c-peptide - what could this be?
hypoglycaemia in a diabetic factitious disaese someone has injected the insulin.
133
Hypoinsulinaemic hypoglycaemia
- fasting/starvation - exercuse etc
134
neonatal hypoglycaemia
hypoinsulinaemic hypoglycaemia go over slide could also be due to inborn error of metabolism e.g. in FA oxidation pathway, would not have ketones
134
neonatal hypoglycaemia
hypoinsulinaemic hypoglycaemia go over slide could also be due to inborn error of metabolism e.g. in FA oxidation pathway, would not have ketones
135
What is the appropriate / inappropriate response in hypoglycaemia?
135
What is the appropriate / inappropriate response in hypoglycaemia?
136
reactive/postprandial hypoglycaemia
137
main reason for hypoglycaemia in anorexia
not enough glycogen stored in liver
138
What is Km? (Michaelis menten constant)
subtrate concentration at which the reaction velocity is 50% of maximum
139
what do elevate serum enzymes point to?
disasesd organ
140
ALP
alkaline phosphatase intra/extrahepatic bile ducts bone placenta (physiological increase in pregnancy) intestine there is also a physiological increase in childhood
141
what happens in ALP deficiency
osteomalacia indicates that it is important for bones
142
What should you also check if there is a raised ALP?
hx check LFTs (GGT and ALT) -> liver check vitamin D -> bone
143
which organs do AST and ALT come from which one is more specific for the liver?
ALT is more specific for liver both found in heart, liver muscle, kidney
144
Raised ALT - what could it be?
hepatocyte damage (toxins, hepatitis, NAFLD, cancer, ischaemia e.g. post cardiac arrest) not really used as a biomarker of kidney, heart or pancreas damage because we have better biomarkers
145
How can you detect intestinal ALP?
usually ALP should not be secreted when you are fasting so get the person to fast and then measure ALP, it should be back to mnromal
146
is raised ALP in a pregnant person worrying
it is normal to have elevated ALP in pregnancy as it is secreted from the placenta
147
gamma-GT
released from liver and biliary system if it is high the problem is in the RUQ can also be increased in response to alcohol or certain drugs
148
LDH
lactate dehydrogenase important for anaerobic metabolism
149
where is LDH found?
WBC RBC Placenta (germ-cell testicular cancer (seminoma)) skeletal muscle (myositis) liver injury cardiac (better biomarkers available)
149
where is LDH found?
WBC RBC Placenta (germ-cell testicular cancer (seminoma)) skeletal muscle (myositis) liver injury cardiac (better biomarkers available)
150
in what cancer is the LDH level proportional to tumour size
151
causes of increased amylase
acute pancreatitis perf duodenal ulcer bowel obstruction *and secondary disease to pancreas salivary gland stones or infection (e.g. mumps) macro-amylase (benign)
152
CK - where is it found?
skeletal muscle cardiac muscle
153
Where is CK used as a biomarker?
rhabdomyolysis myositis polymyositis dermatomyositis severe exercise ........ MI add more not used as a cardiac biomarker anymore because there are better markers (troponin)
154
Troponin I
we measure cardiac troponin elevation indicates damage to cardiac myocytes
155
Reference range of troponin in men and women - same?
no, higher in men because they have bigger hearts
156
What regulates release of BNP?
stretch hypoxia cytokines hormones
157
BNP
b-na... peptide t1/2 18 minutes difficult to measure in blood due to short half life that is why we measure NT-proBNP because it is secreted in equimolar amounts to BNP NT pro BNP is also a lot more stable
158
artiest - drug, what is it and what is it used for?
can cause false low levels of BNP so measure NT-pro-BNP
159
epitope for CAR T cells
CD19
159
epitope for CAR T cells
CD19
160
T-cell markers
CD3+ (all t-cells) CD4 CD8 CD5 immature T cells can be 4+8+ but mature ones are wither 4+ or 8+
161
descrbe spherocytes
smaller than normal RBCs loss of cerntal pallor
162
causes of spherovytosis
- AIHA - hereditary spehrocytosis
163
causes of acquired non-immune haemolytic anaemia
malaria HUS drugs MAHA snake venom drinking anti-freeze
164
Medication for CML
imatinib (Gleevec) it is a tyrosine kinase inhibitor (ABL kinase inhibitor)
165
Blast crisis
chronic leukemia progressing to an acute leukemia transformed as it acquired new mutations
166
Test for polycythaemia vera
Jak2...17 mutation check this!!!
167
which drug to treat CLL?
Ibrutinib
168
what is imatinib?
ABL kinase inhibitor
169
Ibrutinib
brutin tyrosine kinase inhibitor
170
Venetoclax - what is it?
BCL2 inhibito
171
Cause of renal failure in melanoma
cast nephropathy is most likely AL amyloid, hypercalcaemia and ATN are also possible. If there is a very high serum free light chain it is likely to be cast neohropathy, because they can pass through eh basement membrane and precipitate in the tubules
171
Cause of renal failure in melanoma
cast nephropathy is most likely AL amyloid, hypercalcaemia and ATN are also possible. If there is a very high serum free light chain it is likely to be cast neohropathy, because they can pass through eh basement membrane and precipitate in the tubules
172
what FFP do you give in an emergency
AB +/-
173
Who can you give 0+ blood too in emergencies
men and postmenopausal women
174
what would you give in bleeding with low fibrinogen and normal PT/APTT
cryoprecipitate
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