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2nd September [15th-21st Septmber] > Thursday [17/09/2021] > Flashcards

Thursday [17/09/2021] Flashcards

1
Q

Over what age is urine dipstick ineffectual?

A

65

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2
Q

SE of some Abx that can trouble older people especially?

A

GI problems like vomiting and diarrhoea

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3
Q

Define sepsis

A

life-threatening organ dysfunction due ot a dysregulated hoist response to infection

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4
Q

What is SIRS?

A

Systemic inflammatory response syndrome

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5
Q

Parameters for SIRS

A
  1. Temp over 38 or below 36
  2. HR over 90 bpm
  3. RR over 20 or PaCO2 over 32mmHg and
  4. WBC over 12k/cu mm, or >19% immature [band] forms
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6
Q

When was sepsis formally defined?

A

1991

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7
Q

Define sepsis according to the 1991 definition

A

Systemic response to infection, manifested by two or more of the SIRS criteria as a result of infection

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8
Q

Define severe sepsis according to the 1991 definition

A

Sepsis associated with organ dysfunction, hypoperfusion [lactic acidosis, oliguria, or an acute alteration in mental status]

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9
Q

Define septic shock according to the 1991 definition

A

Hypoperfusion despite adequet fluid resuscitation along [lactic acidosis, oliguria, or an acute alteration in mental status]

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10
Q

PP of sepsis

A

Innate immunity and inflammatory mediators

  • activation macrophages, monocytes, neurtrophils and NK cells
  • results in release of proinflammatory cytokines like TNF-alpha, IL-1, IL-6
  • this exagerrated immune response results in collateral damage and death of host cells and tissues
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11
Q

Example of dysregulation of hemostasis

A

Reduced anticoagulation effects of protein C and S
Diminshed fibrinolysis

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12
Q

Example early presentation sepsis

A

Cyanotic dusky peripheries

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13
Q

WHat often supersedes the innital proinflammatory state of sepsis

A

Prolonged state of immunosuppression

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14
Q

Which biomarker can be present early asa sign of immunosuppression sepsis

A

Lymphopenia

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15
Q

How does sepsis work at a cellular level?

A

Decreased delivery and utilization by cells as a result of hypoperfusion
Mitochondrial dysfunction unable to utilise oxygen

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16
Q

What often happens to the heart in sepsis?

A

Acute onset and reversible septic cardiomyopathy 18-60% [TNFalpha and IL-1B]

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17
Q

What does dilation of blood vessels cause?

A

Arterial and venous dilation [induced by inflammatory mediators] -> hypotension and distributive shock + capillary leak -> tissue oedema/ARDS

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18
Q

What often happens to the kidney in sepsis?

A

Reduced renal perfusion, acute tubular necorsis, defects in the microvascular and tubules -> AKI

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19
Q

What often happens to the GI in sepsis?

A

Bacterial translocation across the bowel

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20
Q

What often happens to the liver in sepsis?

A

Cholestasis -> juanidce

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21
Q

What often happens to the brain in sepsis?

A
  1. Septic encephalopathy -> endothelial changes in blood-brain barrier -> entry of toxins, inflammatory cells, cytokines
  2. cerebral odema, NT disruption, oxidative stress, and white matter change -> septic encephalopathy -> mild confusion to delirium and coma
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22
Q

What often happens to the endocrine system in sepsis?

A
  1. sepsis induced catabolism -> to produce amino acids for gluconeogenesis that will feul the immune cells
  2. insulin resistance -> hyperglycaemia
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23
Q

What did the 2016 guidelines do/

A

Removed deifnition of severe sepsis, only septic shock and sepsis now from 1991

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24
Q

New sepsis 2016 guideline

A

Sepsis characterised by life-threatening organ dysfunction due to a dysregulated host repsonse to infection with organ dysfunction base on qSOFA

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25
Q

What is qSOFA?

A
  1. RR of 22+
  2. Altered mentation GCS <15
    3, systolic BP 100 mmHg or less
  3. Score equal or more than 2 = 10% mortality
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26
Q

2016 deinfition of septic shock

A

Hyortension despite adequet fluid resusciation along with:

  • lactic acidosis,
  • oligouria, or
  • an acute alteration in mental status
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27
Q

Hospital mortality septic shock?

A

greater than 40%

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28
Q

Could it be sepsis mnemonic

A

Slurred speech or confusion
Extreme shivering or muscle pain
Passed no urine all day
Severe breathlessness
Illness so bad they fear they are dying
Skin mottled or discoloured

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29
Q

Signs in children of sepsis?

A

Breathing fast child
Has a fit or convulsion
Looks mottled, blush or pale
Has a rash that does not fade when press on it
Is very lethargic or difficult to wake
Feels abnormally cold to touch

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30
Q

What is NEWS used for?

A

National early warning system track and trigger score used ot identify and respond to patients risk of deteriorating

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31
Q

Parameters in NEWS

A

6 parameters

  • HR
  • BP
  • RR
  • O2
  • Temp
  • conscious level
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32
Q

Score for news suspect sepsis?

A

Over 5

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33
Q

RF for sepsis

A

under 1 or above 75, or frail patients
Immuno compromised
- chemo/steroid
- renal failure
- splenectomy
- IVDU
- DM
- indwelling catheters and lines
- post-surgery in 6w
Pregnancy
Neonates

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34
Q

Initial Mx of sepsis

A

ABC
Rapid recognition and resus or patients with sepsis is therefore key to the effective Mx of sepsis
Deteriorating patient siwth NEWS 5 or over should therefore be screened for infection

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35
Q

Initial Ix for sepsis

A
  1. FBC
  2. Clotting profile, with prothrombin time and INR for coagulopathy
  3. U+E -> AKI
  4. LFT -> liver dysfunction
  5. Serum lactate -> hypoperfusion/severity of sepsis
  6. ABG measurement -> acidosis/base deficit
  7. blood cultures
  8. Wound swab
  9. sputum C/S if possible
  10. Urine culture
  11. Lines culutres if there is one
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36
Q

What would raised GAMMA-gt or bilirubin indicate in septic patient?

A

cholestasis

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37
Q

Why should you take take 2 blood cultures?

A

Increases the senstivity for dection of bacteraemia from 70-90%
De-escalate or rationalise antimicrbial therapy

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38
Q

Rate of fluid infusion sepsis

A

Crystalloid 30ml/kg -> 2-3l

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39
Q

Which fluid type preferred septic resus?

A

Crystalloids preferred over colloids
balanced salt solution Hartmann/s, plasmalyte
Say NO to 0.9% saline

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40
Q

Which fluids should give in ARDS?

A

Resrictive fluids

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41
Q

Why should you be careful about fluid overloading the patient in sepsis?

A

Poor outcome for the patient

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42
Q

Which patient group can you use saline for resus in?

A

DKA patient

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43
Q

What are some likely causative pathogens for sepsis?

A

MRSA, VRE, ESBL-enzymes that deactivate B-lactam antibiotics, emergence of CPE due to use of cabapenem

44
Q

RFs for antimicrobial resistance

A

Previous antimicrobial therapy
Previous hospitalisation and
Nursing home resifency

45
Q

How to chose antimicrobial therapy?

A

review previous microbbiology
recently used antimicrbial should be avoided
combination antibiotics in immunocompromised and colonsed resistant strain of bacteria
combination antimicrobial therapy is also recommended in patients with septic shock
find the source and treat the source
- abcess drainage/line reomveal/abdominal patholgoy

46
Q

Which drugs given in chest sepsis?

A

Co-Amox/Tazocin + Clarithromycin look for atypical [pneumococcal/legionella], if ive, stop and give clarithro

47
Q

Which drugs given in urosepsis?

A

co-amox/tazo/mero +/- gentamycin depending on renal function

48
Q

Which drugs given in wound sepsis?

A

Co-amox/Tazocin/Mero/Clindamycin/Vancomycin/Teicoplkanin

49
Q

Which drugs given in line sepsis?

A

mostly G+ve cover teicoplanin/Vancomycin along with G-ve cover Tzocin/Mero

50
Q

Vasopressors to give in sepsis why?

A

increases systemic vascular resistance

51
Q

Vasopressors - give examples fo them

A

Nor-adrenaline [alpha1 and beta1 activity]
Vasopressin
Meteraminol
Phenylephrine

52
Q

MoA of inotropes

A

Increases cardiac contactility

53
Q

Examples of inotropes

A

Dobutamine
Mirinone

54
Q

When to start vasopresors?

A

Start vasopressors if BP is not improving despite adequet fluid resus

55
Q

How to give vasopressors?

A

Nor-adr needs central line
Phenylephrine/metaraminol can be sued peripherally

56
Q

If evidence of myocardial dysfunction what should you give?

A

Dobutamaine/Milrinone via cenrtal line

57
Q

When to give COC?

A
  1. Low dose hydrocortisone 50mg in patients who fail to maintain adequet BP despite fluids and vasopressors
  2. Adrenal gland supression due to sepssi which produce stress homrones including glucocorticoids and mineralocorticoids
58
Q

Effect of COC?

A

Early reversal of shcok
Imporve vasopressors response
However, no strong evidence

59
Q

GLucose control in sepsis?

A

Sepsis/stress induced hyperglycaemia
Insulin resistance

60
Q

What should you maintain glucose levels at in sepsis?

A

Cut-off value of 10mmol/L in sepsis
Avoid hypos and rapid glucose fluctuations

61
Q

How often should you monitor glucose in septic patient/

A

Serum glucose should be measured every 1/2 hours until it is stable, and every 4 hours thereafter

62
Q

What should you not miss in septic patients?

A

eaerly feeding/caloric intake
Stress induced prophylaxis - PPI
DVT prophylaxis
Prevnetion of pressur esores

63
Q

A 71-year-old female with dry age-related macular degeneration is reviewed. Unfortunately her eyesight has deteriorated over the past six months. She has never smoked and is taking antioxidant supplements. What is the most appropriate next step?

Retinal transplant
Intravitreal ranibizumab
Explain no other medical therapies currently available
Photodynamic therapy
Photocoagulation

A

Explain there are no other medical therapies currently available

64
Q

What is the most common cause of sight loss in old people?

A

Age-related macular degeneration is the most common cause of blindness in the UK

65
Q

What is the macula?

A

Central retina

66
Q

Characteristics of ARMD

A

ARMD is characterised by degeneration of retinal photoreceptors that results in the formation of drusen which can be seen on fundoscopy and retinal photography.

67
Q

RFs for ARMD

A

Risk factors
advancing age itself is the greatest risk factor for ARMD
the risk of ARMD increases 3 fold for patients aged older than 75 years, versus those aged 65-74.
smoking
current smokers are twice as likely as non-smokers to have ARMD related visual loss, and ex-smokers have a slightly increased risk of developing the condition, (OR 1.13).
family history is also a strong risk factor for developing ARMD
first degree relatives of a sufferer of ARMD are thought to be four times more likely to inherit the condition.
other risk factors for developing the condition include those associated with increased risk of ischaemic cardiovascular disease, such as hypertension, dyslipidaemia and diabetes mellitus.

68
Q

What are the traditional two types of macular degeneration?

A

Traditionally two forms of macular degeneration are seen:
dry macular degeneration
90% of cases
also known as atrophic
characterised by drusen - yellow round spots in Bruch’s membrane
wet macular degeneration
10% of cases
also know as exudative or neovascular macular degeneration
characterised by choroidal neovascularisation
leakage of serous fluid and blood can subsequently result in a rapid loss of vision
carries worst prognosis

69
Q

Newer, more updated version of ARMD

A

Recently there has been a move to a more updated classification:
early age-related macular degeneration (non-exudative, age-related maculopathy): drusen and alterations to the retinal pigment epithelium (RPE)
late age-related macular degeneration (neovascularisation, exudative)

70
Q

Sx of ARMD

A

Patients typically present with a subacute onset of visual loss with:
a reduction in visual acuity, particularly for near field objects
difficulties in dark adaptation with an overall deterioration in vision at night
fluctuations in visual disturbance which may vary significantly from day to day
they may also suffer from photopsia, (a perception of flickering or flashing lights), and glare around objects

71
Q

Signs of ARMD

A

Signs:
distortion of line perception may be noted on Amsler grid testing
fundoscopy reveals the presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar.
in wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.

72
Q

Ix for ARMD

A

slit-lamp microscopy is the initial investigation of choice, to identify any pigmentary, exudative or haemorrhagic changes affecting the retina which may identify the presence of ARMD. This is usually accompanied by colour fundus photography to provide a baseline against which changes can be identified over time.
fluorescein angiography is utilised if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therapy. This may be complemented with indocyanine green angiography to visualise any changes in the choroidal circulation.
ocular coherence tomography is used to visualise the retina in three dimensions, because it can reveal areas of disease which aren’t visible using microscopy alone.

73
Q

Mx of ARMD

A

Treatment
the AREDS trial examined the treatment of dry ARMD in 3640 subjects. It showed that a combination of zinc with anti-oxidant vitamins A,C and E reduced progression of the disease by around one third. Patients with more extensive drusen seemed to benefit most from the intervention. Treatment is therefore recommended in patients with at least moderate category dry ARMD.
vascular endothelial growth factor (VEGF)
VEGR is a potent mitogen and drives increased vascular permeability in patients with wet ARMD
a number of trials have shown that use of anti-VEGF agents can limit progression of wet ARMD and stabilise or reverse visual loss
evidence suggests that they should be instituted within the first two months of diagnosis of wet ARMD if possible
examples of anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib,. The agents are usually administered by 4 weekly injection.
laser photocoagulation does slow progression of ARMD where there is new vessel formation, although there is a risk of acute visual loss after treatment, which may be increased in patients with sub-foveal ARMD. For this reason anti-VEGF therapies are usually preferred.

74
Q

A 23-year-old woman is referred to the surgical assessment unit. She complains severe, slow onset, left iliac fossa pain. On examination left iliac fossa pain is confirmed. She denies being sexually active. There is some clinical evidence of peritonitis.

Which of the following investigations should you ask for next?

A

Pregnancy test
- in any case of acute abdomen of a female of child bearing age, pregnancy test is madnatory

75
Q

Name some unusual or medical causes of abdominal pain

A

acute coronary syndrome
diabetic ketoacidosis
pneumonia
acute intermittent porphyria
lead poisoning

76
Q

Exam feature of a peptic ulcer

A

Duodenal ulcers: more common than gastric ulcers, epigastric pain relieved by eating
Gastric ulcers: epigastric pain worsened by eating
Features of upper gastrointestinal haemorrhage may be seen (haematemesis, melena etc)

77
Q

Exam feature of a appendicitis

A

Pain initial in the central abdomen before localising to the right iliac fossa
Anorexia is common
Tachycardia, low-grade pyrexia, tenderness in RIF
Rovsing’s sign: more pain in RIF than LIF when palpating LIF

78
Q

Exam feature of acute pancreatitis

A

Usually due to alcohol or gallstones
Severe epigastric pain
Vomiting is common
Examination may reveal tenderness, ileus and low-grade fever
Periumbilical discolouration (Cullen’s sign) and flank discolouration (Grey-Turner’s sign) is described but rare

79
Q

Exam feature of biliary colic

A

Pain in the RUQ radiating to the back and interscapular region, may be following a fatty meal. Slight misnomer as the pain may persist for hours
Obstructive jaundice may cause pale stools and dark urine
It is sometimes taught that patients are female, forties, fat and fair although this is obviously a generalisation

80
Q

Exam feature of a acute cholecystitis

A

History of gallstones symptoms (see above)
Continuous RUQ pain
Fever, raised inflammatory markers and white cells
Murphy’s sign positive (arrest of inspiration on palpation of the RUQ)

81
Q

Exam feature of a diverticulitis

A

Colicky pain typically in the LLQ
Fever, raised inflammatory markers and white cells

82
Q

Exam feature of a abdominal aortic aneurysm

A

Severe central abdominal pain radiating to the back
Presentation may be catastrophic (e.g. Sudden collapse) or sub-acute (persistent severe central abdominal pain with developing shock)
Patients may have a history of cardiovascular disease

83
Q

Exam feature of a intestinal obstuction

A

History of malignancy/previous operations
Vomiting
Not opened bowels recently
‘Tinkling’ bowel sounds

84
Q

How often is the Depo Provera (medroxyprogesterone acetate) injectable contraceptive given?

Every 2 weeks
Every 4 weeks
Every 8 weeks
Every 12 weeks
Every 24 weeks

A

Every 12 weeks

Depo Provera is the main injectable contraceptive used in the UK*. It contains medroxyprogesterone acetate 150mg. It is given via in intramuscular injection every 12 weeks. It can however be given up to 14 weeks after the last dose without the need for extra precautions**

85
Q

main action of depot provera?

A

The main method of action is by inhibiting ovulation. Secondary effects include cervical mucus thickening and endometrial thinning.

86
Q

Disadvantages of depot provera?

A

Disadvantages include the fact that the injection cannot be reversed once given. There is also a potential delayed return to fertility (maybe up to 12 months)

Adverse effects
irregular bleeding
weight gain
may potentially increased risk of osteoporosis: should only be used in adolescents if no other method of contraception is suitable
not quickly reversible and fertility may return after a varying time

87
Q

CIO of depot provera

A

Contraindications
breast cancer: current breast cancer is UKMEC 4, past breast cancer is UKMEC 3

88
Q

Which one of the following is the most common cause of nephrotic syndrome in children?

Minimal change disease
IgA nephropathy
Focal segmental glomerulosclerosis
Chronic pyelonephritis
Infantile microcystic disease

A

Minimal change glomerulonephritis nearly always presents as nephrotic syndrome, accounting for 80% of cases in children and 25% in adults. The majority of cases are idiopathic and respond well to steroids.

89
Q

Define nephrotic syndrome

A

Nephrotic syndrome is classically defined as a triad of
proteinuria (> 1 g/m^2 per 24 hours)
hypoalbuminaemia (< 25 g/l)
oedema

90
Q

Peak incidence nephrotic syndrome?

A

In children the peak incidence is between 2 and 5 years of age. Around 80% of cases in children are due to a condition called minimal change glomerulonephritis.

91
Q

Other features of nephrotic syndrome

A

Other features include hyperlipidaemia, a hypercoagulable state (due to loss of antithrombin III) and a predisposition to infection (due to loss of immunoglobulins)

92
Q

Prognosis of nephrotic syndrome

A

The condition generally carries a good prognosis with around 90% of cases responding to high-dose oral steroids.

93
Q

You are the F1 on an elderly care ward dealing with a patient who was admitted with an exacerbation of COPD which is now resolved. Her recent blood tests are now available and show an abnormal serum potassium of 2.5. You decide to keep her on the ward for further management because of this. On informing the patient of her findings and your decision, she is insistent that she wants to be discharged so she can go home. You explain to her extensively the danger and risk of death associated with leaving her potassium level untreated but she still insists. What is the appropriate action?

A

If someone is competent and has capacity you cannot force them to accept treatment. This question hinges on the patient’s understanding of the risks associated with declining treatment.

It is not acceptable to detain someone under the mental health act because they decline medical treatment.

It is not acceptable to breach confidentiality because a patient declines treatment.

You cannot lie to a patient because they are making a choice you do not agree with.

94
Q

A 45-year-old man presents to the ED with sudden onset pain in his right flank that radiates to his groin, he describes the pain as severe and says he has vomited several times. Urinalysis is carried out and shows microscopic haematuria. An ultrasound is performed which shows right-sided hydronephrosis and a calculus in the right kidney.

What is the preferred immediate management of this patient?

A

Nephrostomy tube
- acute upper urianry tract obstruction is maanged with nephromstomy

The ultrasound shows that this patient has an acute upper urinary tract obstruction, this is managed with either a nephrostomy tube or a retrograde stent insertion. The obstruction needs to be relieved to avoid further damage to the kidneys and while neither of these management options is definitive they can temporarily relieve the obstruction while definitive management is planned

95
Q

What is a nephrostomy tube? How does it work?

A

Nephrostomy is a tube placed directly into the renal pelvis, proximal to the obstruction which travels through the patient’s back and into a nephrostomy bag. This allows the kidneys to continue functioning and for urine to be drained, protecting it from further damage.

96
Q

What is the definitive Tx for hydronephrosis?

A

Extracorporeal shock wave lithotripsy (ESWL) uses targeted sonic waves that break up the stone into smaller fragments, which can then be passed spontaneously. This is potential definitive management, but as this patient has signs of hydronephrosis the immediate concern would be to relieve the pressure on the kidneys.

Or, percutaneous nephrolithotomy for larger renal calculi and can be consdiered after the above has been tried.

97
Q

When would partial nephrectomy be indicated?

A

Typically renal cancer

98
Q

causes of hydronephrosis?

A

Causes of hydronephrosis include:

Unilateral: PACT Bilateral: SUPER
Pelvic-ureteric obstruction (congenital or acquired)
Aberrant renal vessels
Calculi
Tumours of renal pelvis
Stenosis of the urethra
Urethral valve
Prostatic enlargement
Extensive bladder tumour
Retro-peritoneal fibrosis

99
Q

Ix for hydronephrosis

A

Investigation
ultrasound - first-line: identifies presence of hydronephrosis and can assess the kidneys
IVU- assess the position of the obstruction
Antegrade or retrograde pyelography- allows treatment
if suspect renal colic: CT scan (majority of stones are detected this way)

100
Q

Mx of hydronpehrosis

A

Management
Remove the obstruction and drainage of urine
Acute upper urinary tract obstruction: nephrostomy tube
Chronic upper urinary tract obstruction: ureteric stent or a pyeloplasty

101
Q

Varoious effects on the body for sepsis

A
102
Q

SOFA for non-ICU patients

A
103
Q

Hour-1 bundle for sepsis

A
104
Q

What BP should you aim for in sepsis?

A

Above 65mmHg

105
Q

Various causes of abdominal pain within the body?

A
106
Q

What does this CT show?

A

2nd September [15th-21st Septmber] (5 decks)

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