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CP3 Surgery > General surgery 2 > Flashcards

General surgery 2 Flashcards

1
Q

How is sodium and water controlled?

A

RAAS
Decreased effective arterial blood volume leads to decreased renal blood flow at JGA
This stimulates RENIN: At1–>AT2 via ACE

ATII leads to efferent renal artery constriction (increasing GFR), peripheral vasoconstriction, proximal Na+ reabsorption, sympathetic activation and release of aldosterone

Thirst + ADH release

Aldosterone = distal Na+ absorption

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2
Q

What is the net result of RAAS?

A

Increased EABV

Leads to increased stretch of atrial myocardium and release of ANP

ANP vasodilator renal arterioles and decrease RAAS activity - sodium and water excretion

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3
Q

What are the symptoms of dehydration?

A

Mild: headache, lack of energy, tiredness
Moderate: dry mouth, decreased alertness, sunken eyes and muscle cramps
Severe: confusion, disorientation, tachycardia, tachypnoea, low BP

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4
Q

How should dehydration be monitored?

A

Fluid balance chart
Urine output: <1ml/kg/hour = dehydration
Bloods = increased electrolytes, with raised urea

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5
Q

What electrolyte abnormalities can be seen with excessive vomiting

A

Hypochloraemic, hypokalaemic metabolic alkalosis (as gastric acid is lost)
Sodium depleted

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6
Q

What is the treatment of excessive vomiting?

A

0.9% salne to replace the ECF volume as well as KCL (20mmol) to restore potassium levels

metabolic alkalosis will self-correct with restoration of fluid and potassium balance, but U+Es should be frequently checked during treatment

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7
Q

What electrolyte abnormality will a high volume pancreatic/ileal/jejunal/bile fistula show?

A

Fistulas: likely to contain a high bicarbonate level due to their alkaline nature, and thus fluid and bicarbonate replacement is required

Bowel contents after Ampulla of Vater are alkaline in nature

Acidosis displaces potassium from teh cell, so plasma potassium levels may seem elevated when in fact, total body potassium is depleted

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8
Q

What electrolyte abnormality will be seen with diarrhoea?

A

Acute: hyperchloraemia metabolic acidosis with hypokalaemia if profuse
Chronic diarrhoea can cause a metabolic alkalosis

Treatment: ORS or 0.9% saline and 20mmol potassium

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9
Q

How should fluids be prescribed in a closed head injury?

A

General goal in cerebral oedema = maintain a state of euvolaemia to reduce the risk of a secondary brain injury

If patient = haemodynamically stable, 2/3 of maintenance with isotonic fluid is best.
Hypotonic best avoided as they may decrease serum osmolality and increase cerebral oedema

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10
Q

What electrolyte abnormality is seen in acute tubular necrosis?

A

Hyperkalaemia
Hyperphosphataemia
Hypermagnesia

Hyponatraemia
hypocalcaemia
metabolic acidosis

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11
Q

What electrolyte abnormality is seen in dehydration?

A

Isonatraemia, but can be hyponatraemic if hypertonic fluid is being lost, or hypernatraemic if hypotonic fluid is being lost

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12
Q

What is SIADH?

A

Non-physiologic release of ADH which results in decreased water excretion and normal sodium excretion leading to a dilutional hyponatraemia

Investigations show hyponatraemia with normal urea/creatinine.
There is increased urinary sodium giving aaa increased specific gravity of urine

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13
Q

What are the causes of SIADH?

A

Malignancy: small cell lung, pancreas, prostate
CNS disorders: meningoencephalitis, haemorrhage, head injury
Chest disease: TB, pneumonia, abscess
Endocrine disease: hypothyroidism
Drugs: Opiates, psychotropics
Other: Major surgery, trauma, symptomatic HIV

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14
Q

What is diabetes insipidus?

A

Passage of large volumes of dilute urine (>3L/day) due to impaired water resorption by the kidney collecting ducts

Reduced ADH secretion from the posterior pituitary (cranial DI) or impaired response of the kidneys

pathology: hypernatraemia and raised plasma osmolality

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15
Q

What is the effect of congestive cardiac failure on electrolyte abnormalities?

A

neurohormonal adaptation process - activation of the adrenergic and RAAS - salt and water retention

Can get dilutional hyponatreamia due to dietary sodium restriction and inability to excrete water

Hypokalaemia can result from prolonged administration of diuretics, or hyperkalaemia can occur in severe heart failure leading to reductions in GFR, particularly if they are on potassium sparing diuretics / ACEi

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16
Q

What is shock?

A

Acute circulatory failure that compromises tissue perfusion

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17
Q

What are the different types of shock?

A

Hypovolaemia: haemorrhage/dehydration

Distributive: sepsis, anaphylaxis, neurogenic

Cardiogenic: Mi, arrhythmia, valve

Obstructive: passive PE, tamponade, tension pneumothorax

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18
Q

What is Cardiac output?

A

Stroke volume x heart rate

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19
Q

What is BP?

A

Cardiac output x SVR

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20
Q

What is MAP?

A

diastolic BP + (systolic-diastolic)/3

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21
Q

What are the essential features of any kind of shock?

A

Fall in BP by at least 40mmHg (SPB <90)
Tachycardia
Tachypnoea

Hypovolaemic/cardiogenic: cold, pale, clammy with rapid thready pulse and narrow pulse pressure

Septic: hot, flushed, sweaty with a rapid bounding pulse. pulse pressure wide due to vasodilation

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22
Q

What is the effect of shock on the Brain and cerebrum?

A

Autoregulation over MAP of 50-150mmHg

below - patient = agitated, confused, drowsy and eventually unresponsive

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23
Q

What is the effect of shock on the CVS?

A

reduced diastolic pressure leads to inadequate myocardial perfusion, leading to ischaemic calf pain, arrhythmias and eventually infarction

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24
Q

What is the effect of shock to the resp system?

A

increased respiratory rate due to metabolic acidosis

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25
Q

What is the effect of shock to the kidneys

A

Autoregulation over 70-170 but below this - oliguria

impaired renal function

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26
Q

What is the effect of shock on the GI system?

A

Decreased gut motility and nutrient absorption, and decreased ability to sustain normal flora, leading to infection susceptibility

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27
Q

What is the effect of shock on the skin?

A

Blood supply is centralised, giving cool/clammy/mottled peripheral skin

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28
Q

What levels of NEWS require attention?

A

> 3 urgent medical review

>5 critical care team

29
Q

What is SIRS?

A 
2+ of: 
temperature >38.8 or <36
RR >20 or PCO2 <4.3
HR >90
WCC: <4 or >12x109
30
Q

What is sepsis?

A

SIRS + suspected site of infection

31
Q

What is severe sepsis?

A

Sepsis + hypotension or evidence of end organ dysfunction (oliguria, confusion, lactate >3, SpO2 <94%

32
Q

What is septic shock?

A

Severe sepsis with hypotension not responding to fluid resuscitaiton
Results from over activation of the immune system due to infective cause

The first stage is extensive peripheral vasodilatation and this is compounded by endothelial dysfunction causing fluid loss into the interstitial space (hypovolaemic)

33
Q

What is the mx of sepsis?

A

A-E
Sepsis 6:
In: oxygen, fluid, abx

Out: catheter, lactate, cultures

Urgent senior review.
Once stabilised, source control is the next priority

34
Q

What is Anaphylactic shock?

A

Type 1 IgE mediated hypersensitivity reaction, occurring in response to an antigen that the body has previously been sensitised to

Degranulation of mast cells leads to release of vasoactive mediators such as histamine that cause excessive vasodilation of the venous system
This is compounded by bronchoconstriction and laryngeal oedema

35
Q

What is the acute management of anaphylactic shock?

A 
A-E
0.5mg 1:1000 adrenaline (0.5ml) 
repeat every 5 minutes 
Chlorphenamine 10mg IV
Hydrocortisone 200mg IV

?ITU
ECG
Epipen and skin prick

36
Q

What is the management of Hypovolaemic shock?

A 
A-E 
Fluid loss source?? 
Bolus 500ml 
Inotropes if consistently hypotensive 
Tranexamic acid

Class 1-4: 15% 30% 40% 40%

37
Q

What should u do if patient has haemorrhagic shock

A

MASSIVE transfusion protocol: 2222

get delivery of packed cells, fresh frozen plasma and platelets in 2:1:1

38
Q

What is the mangement of cardiogenic shock?

A

A-E
Morphine
Swan-Ganz catheter, central line and arterial line

PCWP low - give 100mg plasma expander every 15 mins
If ok, give inotropic support
renal dose dopamine

39
Q

What is the cause of neurogenic shock?

A

Inhibition of sympathetic outflow from spinal cord, leading to vasodilation

Maybe due to epidural anaesthesia or spinal cord injury above T6
Will present with hypotension and bradycardia not responding to fluid resuscitation so consider the is a mechanism of spinal injury

40
Q

What is the treatment of neurogenic shock?

A

Fluid resuscitation and vasopressors

41
Q

How are spinal shock and neurogenic shock differentiated?

A

Spinal shock is a transient ‘concussion’ of the spinal cord, leading to flaccid arreflexia, that resolves as the soft tissue swelling decrease
There may be priapism, and there will be no reflexes below the level of injury

42
Q

What is the ‘triad of death’ in bleeding?

A

Coagulopathy
Hypothermia
Metabolic acidosis

bit of a vicious cycle - hypothermia leads to coagulopathy as the clotting factors cannot work effectively, which leads to a metabolic acidosis which then leads to decreased myocardial performance and further hypothermia

43
Q

What are the risk factors for wound infection?

A

General factors: Age, malnutrition, immunosuppression, malignancy, obesity, hypoxia, anaemia

Local factors: type of surgery (clean vs contaminated), length of procedure, residual local malignancy, foreign body insertion, ischaemia

Microbiological factors: lack of antibiotic prophylaxis, virulence of the organism

44
Q

What are the types of surgical site infection?

A

Superficial incisional SSI: infection of the skin and subcutaneous tissue of the incision (most common)

Deep incisional SSI: infection also involving deep tissues such as muscle / fascial layers. This includes organ / space SSIs draining through the incision

Organ / space SSI: infection involving any site involved in the operation, other than the incision

45
Q

Who needs prophylactic antibiotics?

A

Patients at high risk of infection, or in whom the risk may be low but the consequences of an infection would be serious

46
Q

What factors need to be considered in prescribing prophylactic antibiotics?

A

Operative factors: contaminated/dirty surgeries
Patient factors: immunosuppression, previous foreign body implants, heart valve disease or peripheral vascular disease

Choice of abx

Dose and timing factors e.g. highest tissue concentration required at the moment of tissue contamination (IV administration at moment of incision)

Often 2 further doses are given at appropriate times (24 hour Course)

47
Q

What is impetigo?

A

Superficial purulent infection caused by staph aureus, with a characteristic golden crust on an erythematous base
Should always be swabbed, and treatment = topical mupirocin / fusidic acid

48
Q

What is ecthyma?

A

Purulent skin infection caused by staph/strep characterised by ulceration under a crust

Associated with poor hand hygiene and malnutrition (commonly seen in drug addicts)

49
Q

What is erythrasma?

A

Mildly itchy eruption between the toes or in the flexures, caused by Corynebacterium (fluoresces pink with Wood’s light)
Treatment is topical miconazole or oral erythromycin

50
Q

What is folliculitis?

A

Generally caused by staph, and pustules heal in 7-10 days in superficial folliculitis (oral flucloxacillin). Deep folliculitis most commonly occurs in adolescence, with furuncles and carbuncles developing, needing longer courses of tetracycline / erythromycin

51
Q

What us staphylococcal scalded skin syndrome?

A

Fever, irritability and skin tenderness before erythema and skin blistering develops after 24-48 hours, due to toxins from a focus of infection with S aureus. This most commonly occurs in children and a bacterial swab should be taken from the nose/throat with immediate IV flucloxacillin started alongside supportive measures

52
Q

What is cellulitis?

A

Infection of subcutaneous tissue, most commonly due to streptococcal infection
Erysipelas is more superficial dermis infection, often with a raised erythematous edge and affects the face

53
Q

What are viral warts?

A

Smooth, skin-coloured papules that enlarge to have an irregular hyperkeratotic surface.
Usually resolve spontaneously

54
Q

What is molluscum contagiosum

A

poxvirus leading to classically umbilicate papules that resolve spontaneously over many months

55
Q

What is ringworm?

A

Erythematous annular lesions with central clearing, with treatment generally topical terbinafine or ketoconazole, however, systemic terbinafine or itraconazole may be needed in widespread disease

56
Q

What are scabies?

A

Diagnosis made by identifying the scabietic burrow, usually on the edges of the fingers or sides of the hands/feet.

Topical treatment (permethrin/malathion) is required for all physical contact

57
Q

What is the cause of anaerobic gangrene?

A

Clostridium per fringes found in soil/faeces
Can arise from trivial injury, often in immunocompromised patients

Initially gas in the tissues and skeletal muscle (crepitus) with oedema and spreading gangrene plus systemic upset

58
Q

What is the management of anaerobic gangrene?

A

May need resuscitation

Aggressive debridement and IV penicillin + metronidazole

59
Q

What is synergistic gangrene?

A

Aerobes and synergistic anaerobes infect an initial wound / surgical site, leading to severe wound pain and gas in the tissues
There may be extensive subdermal gangrene

60
Q

What is the treatment of synergistic gangrene?

A

Debridement, antibiotics and systemic support

61
Q

What is the cause of mild pyrexia post-operatively?

A

response to tissue injury and stress

62
Q

What should be done when reviewing the patient with post-op pyrexia?

A

Review general observations, urine output
Insepct the wound for superficial infection/haematoma
Inspect cannula sites for thrombophlebitis/infection
Examine the chest to exclude infection, infarction or acute heart failure
Examine the legs for DVT
Consider other sources of infection e.g. urine/GI infection

63
Q

What is a routine isolation unit used for?

A

To protect other patients / staff from a patient’s infection e.g. TB (special masks also required) and MRSA

64
Q

What is a reverse isolation unit used for?

A

Protect patients from getting an infect carried by staff/visitors / other patients
These are used in those with decreased natural immunity e.g. transplant recipients, chemotherapy patients

65
Q

What are the common locations of intra-abdominal abscess?

A

Alongside the organ or origin e.g. parabolic, parapancreatic

Pelvic e.g. post-pelvic sepsis (appendicitis)

Subphrenic e.g. post GI perforation

66
Q

What are the general clinical features of intra-abdominal abscess?

A

Malaise, anorexia, swinging pyrexia, tachycardia and a possible mass

67
Q

How is intra-abdominal abscess diagnosed?

A

CT abdo / pelvis
Management: IV empirical Abx as well as radiologically (CT/USS) guided drainage where possible
Surgical drainage is a last line measure

68
Q

What are the steps of drainage of a superficial abscess?

A

Often performed under GA
Point of maximum fluctuance is incised and then blunt probing ensures all loculi are drained

Small abscesses - dry dressing, whereas deeper abscessed require frequent packing with antiseptic ribbon gauze / use of a corrugated drain to keep them open until they have filled with granulation tissue

CP3 Surgery (12 decks)

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