Critical Care Flashcards
(170 cards)
1
Q
Which two nerves can be damaged in a thyroidectomy?
A
Recurrent laryngeal
External laryngeal
2
Q
What results from damage to external laryngeal nerves?
A
Loss of high pitched voice
3
Q
What happens when you damage the Recurrent laryngeal nerve?
A
Unilaterally; partial - asymptomatic, dyspnea on exertion complete - hoarseness and aspiration
Bilaterally partial - acute sob and stridor, complete - speech lost and aspiration
4
Q
Clinical picture of hyperthyroidism
A
Weight loss
Heat intolerance
Sympathetic stimulation - peripheral tremor, AF, anxiety, irritability, insomnia
Eye signs - lid lag, exophthalmos, diplopia
Pretibial myxoedema
5
Q
Role of thyroid hormone
A
Increase BMR
Protein metabolism
Carbohydrate metabolism- all increased
Fat metabolism
Increase CO
6
Q
How is T3 and T4 synthesised
A
Active pumping
Oxygenation
Iodination
Coupling
Intrathyroidal de-iodination
Secretion
7
Q
Clinical picture of thyroid crisis
A
Hyperpyrexia
Tachycardia, arrhythmia, hypotension, tschypneoa
Agitation , anxiety, delirium
Vomiting diarrhoea
Death
8
Q
Management of thyroid crisis
A
Supportive - correct electrolytes, fluids
Medicationz - b- blockers, thionamide, iodine solution, cholestyramine- prevents hormone reabsorption
9
Q
What is a steroid
A
Biologically active organic compound with four rings arranged in specific molecular configuration
10
Q
What is an addisonian crisis
A
Critical condition due to an acute reduction of circulating steroids. Due to- adrenal insufficiency (Addisonian disease), sudden cessation of corticosteroids after prolonged course, Stress conditions (surgery trauma infection) in those with underlying addisonian disease or steroid therapy
11
Q
Clinical presentation of addisonian crisis
A
Sudden severe abdo pain
Nausea, vomiting, diarrhoea = dehydration
Unexplained shock, unexplained hyper/hypothermia
Hyponatraemia, hyperkalaemia, metabolic acidosis, hypoglycemia
12
Q
Management of addisonian crisis
A
Management as per CCRISP protocol (a-e) in ITU
Immediate 100mg IV/IM hydrocortisone
24 hrs cont 100-200mg IV hydrocortisone in 5% glucose
1L normal saline in 1 hour, 4-6L in 24hrs
Adjust metabolic disturbances
13
Q
Wallace rule of 9s for burns
A
Head and neck (front and back) 9%
Upper limbs each 9%
Trunk front and back 36%
Lower limbs each 18%
Genitalia 1%
14
Q
Burn initial management
A
ATLS protocol A-E approach
A- look for signs of inhalational injury/burn, consider intubation
B- Ensure adequate ventilation, tracheal and pulmonary burns can impair gas exchange, chest burns may impede chest expansion
C- 2 large bore cannula and IVI calculated using Parkland formula, urinary catheter
15
Q
What is the Parkland formula
A
Total fluid in 24hrs for burns patient = 4ml x total burn surface area % x body weight kg
50% in first 8 hours 50% in next 16
Aiming for urine output of 0.5-1 ml/kg/hr in adults
16
Q
Why do you not give colloidal in burns?
A
Colloids will pass to extravasculat space due to increased capillary permeability occurring in first 24hrs, therefore exerting an oncotic effect and cause a paradoxical augmentation of the 3rd space
17
Q
Complications of burns
A
Shock - hypovolaemia due to loss of skin cover, hypotension, tachycardia, increased SVR, fall in CO
Sepsis, ARDS
Renal failure
Circumferential burns require escharotomy
Electrolyte disturbance
Coagulopathy (hypothermia, DIC)
Haemolysis
18
Q
How to tell if burn is deep or superficial
A
Superficial- partial thickness = red/white, blistering, sensate
Deep - full thickness = white, leathery, desensate
19
Q
Define ARDS
A
Acute diffuse inflammatory lung injury
Characterised by hypoxemia, diffuse pul infiltrates on CXR, normal PAWP, pao2/fio2 <26.6
20
Q
Pathophysiology of ARDS
A
Two phases.
Acute phase -
Widespread destruction of capillary endothelium, extravasation of protein rich fluid, interstitial oedema
Neutrophil migration and cytokine release
V/Q mismatch from alveolar basement membrane damage
Late phase-
Fibroproliferation
Lung scarring
21
Q
Berlin criteria
A
New definition for ARDS
Mild, moderate, severe
22
Q
Management of ARDS
A
ITU, supportive therapy, treat underlying cause
Ventilation- PEEP & prone
Steroids - low dose
Sepsis- treat
Fluids
Nutritional support
23
Q
Long term sequels of ARDS
A
Impaired gas exchange - v/q mismatch, shunting
Decreased lung compliance.
Pul HTN
24
Q
Portosystemic anastomosis
A
Oesophagus
Rectal
25
When do you CT head for trauma?
High risk
Gcs < 15 at 2 hrs post injury
Suspected open or depressed skull #
Sign of basillar skull #
2+ vomiting episodes
Over 65
On anticoag
Medium risk
Retrograde amnesia
Dangerous mechanism
26
Signs of basilar skull #
Haemotympanum
Raccoon eyes
Battles sign
Csf oto/rhinorrhea
27
Normal ICP
7-15 mmhg
28
Ways to measure ICP
Intraventricular catheter - gold standard, allows csf drainage, high infection rate
Intraparenchymal or subarachnoid probe
Epidural probe
Lumbar csf pressure
Tympanic membrane displacement
29
Cushing reflex
Physiological response to raised ICP = cushings triad. Widening pulse pressure, irregular breathing,
Hypertension, bradycardia
30
Pathophysiology of raised ICP
Monro-Kellie doctrine
Skull is a fixed box
Balance between blood, brain, csf
Increase in one, results in decrease of the other to prevent icp rise
At approx 25mmhg, small brain volume increase results in icp raise
Loss of compensation ability = brain herniation
31
Presentation of ICP
Headache
Nausea, vomiting
Papilloedema
Fall in GCS
Dilated pupil
Lateral gaze defect
Cushing triad
32
Indications for intubation in brain injury
Gcs < 8
Raised icp risk due to agitation
Inability to maintain or protect airway
Seizures
Severe facial injuries
33
Mx of raised ICP
Elevate bed to 30 degrees
Good neck alignment +/- immobilisation in sandbags/blocks, not collar. Collar increases ICP
Mannitol, occasionally hypertonic saline
Furosemide
Na 140-145
Avoid hyperthermia
Sedation
Hyperventilation to reduce PaCO2 as temporary measure
Decompressive craniectomy
Extraventricular drain
34
SDH CT scan
Crescent shape hypertension lesion
35
What is “GCS”?
Glasgow Coma Scale is a neurological scale which aims to give a reliable and objective way of recording the conscious state of a person for initial as well as subsequent assessment.
36
Management of Acute SDH
Neurosurgical Review once immediate resuscitation is completed.
Consideration of surgical management vs non-surgical management.
Surgical = haematoma evacuation - considered if coma, midline shift, neurological deterioration
Non-surgical = monitored in ITU, serial CT scans, monitoring for neurological deterioration
37
management of airway and breathing in ATLS protocol
Airway & c-spine
secure and patent, not at risk, if not speaking - look for foreign bodies, facial trauma, check breathing on cheek and listen to breath sounds
chin lift/jaw thrust
airway adjunct
cricothyroidotomy, intubation
triple immobilisation of c-spine with blocks, tape & collar, or inline stabilisation
breathing
assess chest wall deformity, paradoxical breathing, flail chest, rise & fall of chest, Respiratory rate
assess equal chest expansion, central trachea, surgical emphysema
percuss & auscultate need to ensure no tension pneumothorax
manage with high flow O2 with non rebreathe mask, needle thoracostomy or chest drain
38
How do you manage a tension pneumothorax?
urgent needle thoracostomy in 4th or 5th intercostal space anterior to the midaxillary line then chest tube insertion
39
How do you manage circulation as per ATLS?
Assess perfusion centrally & peripherally
Assess radial pulse - rate rhythm character
Assess BP & urine output
listen to Heart sounds
check long bones & pelvis for bleeding
2 large bore cannula
IV Fluids, activate MHP, TXA long bone splinting, pelvic binder
40
Four areas for a FAST scan to assess
perihepatic space
perisplenic space
pericardium
pelvis
41
Grades of Liver tear
Graded 1 to 6
by AAST
Graded 1 to 4 by WSES
4 = unstable
42
Define shock
state of cellular and tissue hypoxia due to reduced oxygen delivery and or increased oxygen consumption or inadequate oxygen utilisation
43
Types of shock
Hypovolaemic
Septic
Anaphylactic
Cardiogenic
Neurogenic
44
What is the difference between spinal shock and neurogenic shock?
Spinal shock - immediate temporary loss of total power, sensation and reflexes below injury level
Neurogenic - loss of sympathetic nervous system signals
both have hypotension and bradycardia
45
Agents given in neurogenic shock
phenylephrine hydrochloride
dopamine
norepinephrine
46
What spinal cord syndromes are there?
Central
Anterior
Brown-sequard
47
What is central cord syndrome?
- greater motor loss in upper extremities than lower, variable sensory loss
- hyperextension injury in someone with pre-existing canal stenosis
48
What is anterior cord syndrome?
- paraplegia
- bilateral loss of pain & temperature sensation
- sensation from dorsal column ( vibration, proprioception, pressure) in tact
- after cord ischaemia
49
What is Brown Sequard Syndrome
- ipsilateral motor loss (corticospinal tract), loss of proprioception with contralateral loss of pain & temperature (spinothalamic) below injury level
- from cord hemi-section
50
Corticospinal tract
ipsilateral motor control
tested by muscle movements, response to painful stimuli
51
Spinothalamic tract
Contralateral temperature and pain
tested by pinprick
52
Dorsal columns
Ipsilateral proprioception, vibration, some light touch
test position of toes or vibration using tuning fork
53
Types of pelvic fracture
Anterior-posterior
Lateral compression
Vertical shear
Complex - combination of patterns
54
How do you confirm urinary bladder injury?
Anterograde cystourethrogram
Retrograde urethrogram
55
Contraindication to catheterisation
Pelvic fracture
blood on urethral meatus
perineal haematoma
pre-existing infection around glans or meatus
meatal stenosis
56
Advantages of whole body CT
rapid identification of trauma
look for extent of disease/trauma
57
disadvantages of whole body CT
timely, expensive
radiation exposure
58
What are the causes of narrow pulse pressure?
Hypovolaemia
loss in circulating blood volume = low systolic and therefore, increase in SVR and an increase in vasomotor tone therefore increasing diastolic, narrowing pulse pressure
59
How do you manage a pelvic fracture?
BOAST guidelines
Resuscitate patient using ATLS A-E approach
Pelvic binder
TXA & MHP
CT imaging with IV contrast
packing or IR
Ex-fix
urinary injuries managed as per BOAST with urology
check for wounds, if open = manage as per BOAST open fracture guidelines
reconstruct pelvic ring in 72 hours
60
Clinical picture of compartment syndrome
Pain+++ despite high dose analgesia
raised compartment pressure
tense & tender compartments
pain on passive stretch
paraesthesia and loss of pulses = late sign
61
Normal compartment pressure
0-15mmHg
62
Why do you get acute renal failure in compartment syndrome?
Nephrotic effect of myoglobulin precipitating in renal tubules
Decrease ECF = vasoconstriction
Renal tubular ischaemia & necrosis
myoglobulin, uric acid = obstructive cast formation
63
What is myoglobin?
O2 binding protein in muscles
64
Define Rhabdomyolysis
Release of toxic muscle cell components into systemic circulation
muscle breakdown = release of intracellular contents - results in acute tubular necrosis in kidney and causes increase CK and dark reddish urine
65
Causes of rhabdomyolysis
Blunt trauma, ie crush injury
compartment syndrome
massive burns
Drugs - statins, alcohol
ischaemic reperfusion injury
strenuous exercise
66
Blood results of rhabdomyolysis
Increased CK > 5x normal
increased lactate
hyperkalaemia
hypocalcaemia
high phosphate and uric acid
67
management of rhabdomyolysis
A-E
IVF
treat electrolyte disturbances
monitor ECG
diuretics
68
Causes of thrombocytopenia
Hypersplenism
DIC
haemodilution
Chronic low platelet production
69
Indications for platelet transfusion
ongoing coagulopathy with continued bleeding
low platelets pre-operatively
70
Blood results in alcoholics
Macrocytic anaemia
thrombocytopenia
elevated liver enzymes - GGT, AST, ALT, ferritin
deranged clotting, raised INR
71
Sites of portosystemic anastamosis
lower oesophagus
upper anal canal
umbilical
72
Varices that usually bleed
those in submucosa of lower oesophagus
73
pathogenesis of portal HTN in chronic alcoholics
alcoholic liver disease - cirrhosis - fibrosis obstructing portal venous return, causing portal HTN to develop
74
Alternatives to medication to treat portal HTN
Portosystemic shunts - TIPSS - stent inserted via transjugular route
stapled oesophageal transection
Liver transplant
75
How does alcohol cause cirrhosis?
changes in lipid metabolism
decreased export of lipoproteins
cell injury caused by reactive oxygen species and cytokines
76
Hepatic changes as a result of alcohol consumption
Fatty change
alcoholic hepatitis with liver cell damage
cirrhosis
hepatocellular carcinoma
77
How is alcohol metabolised by the liver?
microsomal ethanol oxidising system enzymes
alcohol dehydrogenase
catalase reaction
all metabolise ethyl alcohol to acetic acid
78
mechanism of ascites
increased formation of hepatic and splanchnic lymph
low albumin
increased aldosterone and ADH = salt & water retention
79
How does vit B12 deficiency cause macrocytic anaemia?
Vit b12 = DNA synthesis
if impaired - cell cycle cannot progress from G2 growth to Mitosis stage
therefore, cont cell growth without division
= macrocytosis
80
Counselling for liver transplant
lifestyle modifications - abstain from alcohol
ABO matching
immunosuppression
81
indication for sengstaken tube placement
acute life threatening bleeding from oesophageal or gastric varices that doesn't respond to medical therapy and endoscopic haemostasis isn't available
82
What are the ports of a sengstaken blakemore tube?
gastric balloon
oesophageal balloon
gastric suction
83
CXR findings with perforated gastric/duodenal ulcer
air under diaphragm
84
Risk factors for perforating PUD
NSAIDS
steroids
H.pylori
previous peptic ulcers
malignancy
85
How do NSAIDS cause peptic ulceration?
1. topical irritant effect of these drugs on the epithelium
2. impairment of barrier properties of the mucosa
3. suppression of gastric prostaglandin synthesis through inhibition of cyclo-oxy-genase
4. reduce gastric blood flow
5. interference with repair of superficial injury
86
MOA of PPI
PPI binds irreversibly to H/K ATPase enzyme (proton pump) on GASTRIC PARIETAL cells
blocks H ion secretion therefore unable to bind with Cl to make HCl
87
Actions of HCL
1. activates pepsinogen to pepsin (proteolysis)
2. Antimicrobial
3. stimulates small intestinal mucosa to release CCK and secretin
4. promotes Ca2+ absorption in small intestine
88
What are the phases of gastric secretion?
1. Cephalic phase
2. Gastric phase
3. Intestinal phase
89
What happens in cephalic phase of gastric secretions?
30% acid produced
vagus stimulation causing secretion of HCl and gastrin release from G cells
90
What happens in the gastric phase of gastric secretions?
60% acid produced
stomach distension/low H+/peptides = gastrin release
91
What happens in the intestinal phase of gastric secretion?
10% acid produced
high acidity/distension/hypertonic solutions in duodenum inhibit gastric acid secretion via CCK, secretin and neural reflexes
92
Surgery classifications NCEPOD
1 - immediate/lifesaving
2 - urgent life threatening/limb threatening
3 - expedited
4 - elective
93
why do you get hyponatraemia in metabolic alkalosis
kidneys excrete NaHCO3 to reduce blood alkalinity = hyponatraemia
94
Why do you get paradoxical aciduria with hyponatraemia in metabolic alkalosis?
hyponatraemia = RAAS stimulation = more Na & H2O reabsorption in exchange for H & K = hypokalaemia and urine increases acidity due to H+
95
Clinical picture of hyponatraemia
confused
agitation
fits
low GCS
96
Causes of hyponatraemia
Depletional - diarrhoea, diuretics, burns
Endocrine - Addisons, hypothyroid
SIADH
Multiple myeloma
HF
97
How does bilirubin circulate within the plasma?
- free bilirubin
- conjugated to glucuronic acid
98
Why do you get clotting derangement in liver disease/pathology?
liver synthesises most clotting factors
severe liver damage / biliary obstruction = decreased absorption of Vit K
Vit K needed for clotting factors 1972
99
What clotting studies may be abnormal in liver conditions?
increased prothrombin time
or INR
100
how to correct clotting abnormality?
IV Vit K
FFP
Prothrombin complex
haematologist
101
What is alkaline phosphatase?
- enzyme in epithelium of bile canaliculi
- in bone, placental tissue
- increases in cholestasis to a far greater extent than ALT, AST
- ALT, AST in hepatocytes and increase = liver damage rather than obstructive jaundice
- ALT > AST = liver pathology
102
What is the function of bile?
Emulsification of fat into micelles = greater surface area for action of pancreatic lipase enzyme
103
How do bile salts help in emulsification of fat?
bile salt anions are hydrophilic on one side & hydrophobic on the other
aggregate around lipid droplets to form micelles
hydrophilic sides are negatively charged & charge prevents fat droplets coated with bile from re-aggreagating into larger fat particles
104
Constituents of bile
water
cholesterol
lecithin
bile pigments
bile salts and bile acids
copper and excreted metals
105
what is bilirubin conjugated to?
in liver conjugates with glucuronic acid by
glucuronyl transferase
106
Bilirubin metabolism
- conjugated bilirubin = secreted into bile and enters small intestine, passes into colon
- in the colon - gut bacteria convert conjugated bili into urobilinogen - some reabsorbed into blood, some reenters liver or excreted by kidneys as urobilin = wee yellow colour
- majority or urobilinogen is oxidised to stercobilin = excreted in faeces = brown colour
107
Causes of Jaundice
Pre-Hepatic - haemolytic anaemia (Sickle cell, G6PD), Gilbert's
Hepatic - ALD, viral hepatitis, PBC, Hepatocellular carcinoma
Post-Hepatic - gallstones, cholangiocarcinoma, pancreatic cancer, drug induced
108
Glasgow Scoring system for pancreatitis
P - aO2
A - ge > 55
N - eutrophils > 15
C -alcium <2mmol
R -enal (urea) - >16mmol
E -nzymes (LDH > 600)
A -lbumin < 32
S - ugar (glucose >10)
3+ =severe = ITU
109
Pancreatic scoring systems
Glasgow
Ranson's
Balthazar CT scoring
APACHE
110
What can be the course of normal amylase in pancreatitis?
- returns back to normal after 48Hrs
- not specific for pancreatitis
can occur in SBO, tubo-ovarian disease, mesenteric ischaemia
- doesn't correlate to severity of pancreatitis
111
Why do you get hypocalcaemia in pancreatitis?
Early - autodigestion of mesenteric fat by pancreatic enzymes, release of free fatty acids, form calcium salts, transient hypoparathyroidism and hypomagnesaemia
Late - due to sepsis complications = increase catecholamines = shift in circulating calcium into intracellular compartment = relative hypocalcaemia
112
pathophysiology of hyperglycaemia in pancreatitis
pancreatic enzymes destroy B cells of islets of langerhans = increase in serum glucose
stress response
113
How do you manage nutrition in pancreatitis?
TPN is usually needed
consider NJ tube feeding
consider premorbid nutritional status & current nutritional needs
114
What are the complications of pancreatitis?
Local - pseudocyst, necrosis, bleeding, renal failure
Systemic - hypovolaemic shock, haemorrhagic, MOF, ARDS
115
Treatment for splenic vein thrombosis
LMWH
MDT approach - gastro, haem, IR, surgeon
116
Endocrine function of the pancreas
Alpha cells - glucagon
Beta - insulin
Delta - somatostatin
PP - pancreatic polypeptide
117
Exocrine function of pancreas
Pancreatic enzymes for digestion of fat, carbs, proteins
- lipase
- amylase
- enterokinase (trypsinogen to trypsin)
118
causes of acute pancreatitis
gallstones
alcohol
trauma
post ERCP
infection (mumps)
119
pathogenesis of pancreatitis
duct obstruction = bile reflux = injury & damage to pancreatic acini = leakage of pancreatic enzymes = damage
trauma, drugs, infection can also damage acini
lipase = fat necrosis
elastase destroys blood vessels
120
CT findings in acute pancreatitis
oedema
fat stranding
collection/abscess
necrosis
pseudocyst
121
Mx of pancreatitis
A-E
IVF
Hx & exam
Bloods
USS/CT
ITU
analgesia
NGT, urinary catheter
122
What is the role of corticosteroids in pancreatitis?
- suppress the release of inflammatory cytokines
- can reduce LOS and the need for surgical intervention in severe pancreatitis
123
What Abx are used in acute pancreatitis?
carbapenem
quinolone
(penetrate pancreas)
124
How do you manage pain in pancreatitis?
WHO Pain ladder
Simple analgesics
mild opioids
strong opioids, PCA, epidural
pethidine/meperidine
125
Define pseudocyst
collection of amylase rich fluid enclosed in wall of fibrous or granulation tissue
126
What is the commonest site of pseudocyst in pancreatitis
lesser peritoneal sac in proximity to pancreas
127
What symptoms come with a pseudocyst?
epigastric swelling
dyspepsia
vomiting
mild fever
128
What are complications of pancreatic pseudocyst?
Infection - abscess/sepsis
Rupture - GI bleed, peritonitis
Enlargement - biliary compression, jaundice, bowel obstruction
129
difference between true pancreatic cyst and pseudocyst
pseudocyst isn't closed and doesn't have lining of epithelial cells
130
Management of pancreatic pseudocyst?
40% resolve in 1/52 with supportive mx
cysto-gastro-stomy to remove if persists over 2 months, or infected, or enlarges
131
How does paracetamol overdose cause liver injury
toxic metabolite N A P Q I is neutralised by glutathione, with excess paracetamol taken, not all NAPQI is neutralised and accumulates in the liver, damaging it
132
Define shock
circulatory failure resulting in adequate organ perfusion
133
define septic shock
sepsis with hypotension or hypoperfusion resulting in organ dysfunction despite fluid resus
134
Basic principles of septic shock mx
Respiratory support - O2, NIV, ETT for ARDS/respiratory failure
Circulatory support - IVF, Inotropes
Renal support - output > 0.5ml/kg/h
nutritional support
Broad spectrum ABx until sensitivies back
135
Mx of diverticular abscess
Open drainage - good wash & stoma option
Image guided aspiration - less adequate drainage, reduced wound infection risk, and LOS
136
what is thumbprinting a sign of on AXR?
large bowel wall thickening
related to infective or inflammatory colitis
137
DD of bloody diarrhoea
UC, Crohn's
ischaemic colitis
Carcinoma
Infective colitis by c diff
138
How do you investigate bowel symptoms
FBC, U&E, CRP
ESR
CEA
Stool analysis and culture
antibodies for IBD
Colonoscopy
139
Indications for urgent surgical mx of bloody diarrhoea
toxic megacolon refractory to medical management
uncontrolled colonic bleeding
perforation
obstruction & stricture with cancer suspicion
140
What is the surgical mx of bloody diarrhoea
pan-proctocolectomy with ileostomy
141
What do you expect in an ABG with intestinal obstruction?
metabolic acidosis
142
What are the factors affecting tissue oxygenation?
C.O. x CaO2 x 10
143
factors influencing haemoglobin affinity for oxygen
Shifts to the Left = lower oxygen delivery
Low H ions (alkali)
low pCO2
low 2,3-DPG
low temp
HbF, carboxyhaemoglobin
Shifts to the Right = higher oxygen delivery
raised H (acidic)
raised pCO2
raised 2,3-DPG
raised temp
144
How do you investigate microcytic hypochromic anaemia?
total iron binding capacity
ferritin
occult blood in stool
145
What is an enterocutaneous fistula?
abnormal communication lined by granulation tissue between skin and GIT
146
How can you classify enterocutaneous fistulae?
congenital/acquired
internal/external
simple/complex
location
output
147
Predisposing factors to an enterocutaneous fistula
intestinal anastomosis
crohn's
infection
cancer
irradiation
ischaemia
148
Signs of intrabdominal sepsis
local - peritonitis, abdo pain, vomiting, guarding
systemic - fever, hypotension
149
Management of intrabdominal sepsis from enterocutaneous fistula
Sepsis control
MDT approach
Nutritional support
IVF
electrolyte correction
surgery planned
protect skin
150
151
factors preventing healing of enterocutaneous fistula
malignancy
infection
crohns
malnutrition
high out
152
What does a fistulogram tell you
track length
locates fistula
locates distal obstruction
153
Layers of the adrenal cortex
GFR - salt, sweet, sexy
Zona Glomerulosa - aldosterone
Fasciculata - cortisol
Reticularis - sex hormones
154
Actions of aldosterone
Na+ reabsorption
K+ excretion
Water balance with salt & water retention
Acid base balance with K+ excretion
155
Cortisol actions
Anti-insulin effect = increases blood glucose
stimulates gluconeogenesis = increases CBG
stimulates protein synthesis in liver
stimulates lipolysis
anti-inflammatory
immunosuppressive
156
What advice do you give to someone starting steroids?
- many side effects
- don't stop suddenly
- make drs aware if you're admitted to hospital - steroid card/bracelet
- increased infection risk
- delayed wound healing
- weight gain
- OP
- increased CBG
- muscle weakness
- mood/behaviour changes
- risk of ulcers, no NSAIDS
157
post-thyroidectomy hypocalcaemia
removal or ischaemia of parathyroid glands
158
how is ca2+ transported in the blood
50% unbound & ionized
45% bound to plasma proteins
5% associated with anions (citrate and lactate)
159
Role of Ca2+
NEUROMUSCULAR Transmission
smooth and skeletal muscle contraction
cardiac & nerve function
co-factor for blood coagulation steps
bone mineralisation
160
Hormones involved in Ca2+ homeostasis
PTH - increase calcium
Vit D3 - calcitriol - increases serum calcium
Calcitonin - stimulates excretion
161
Function of PTH
Bone - stimulates osteoclasts - therefore increases bone reabsorption = increase serum calcium
Renal - increases calcium reabsorption in the kidneys reducing calcium loss in urine
promotes Vit D into calcitriol increasing calcium absorption from the intestines
162
How is vit D3 formed?
Sunlight + 7-de-hydro-cholesterol = previtamin D3
163
Signs of hypocalcaemia
CATS go numb
Convulsions
Arrythmias
Tetany
Spasms and stridor
finger numbness
164
Which muscle are you concerned about in tetany?
laryngeal muscle
165
how do you treat hypocalcaemia tetany?
cardiac monitoring
10ml 10% calcium gluconate
IVF
166
Type of anaemia in hypothyroidism
macrocytic anaemia
167
How is T3 & 4 synthesised
Iodide ions enters thyroid follicular cells by ACTIVE Pumping
Iodide converted to iodine by TOP
iodine + tyrosine = mono-iodotyrosine & diiodotyrosine (MIT & DIT)
MIT + DIT = T3
DIT + DIT = T4
168
hypothyroid causes
primary -
surgery, drugs
autoimmune
iodine deficiency
transient thyroiditis
secondary -
pituitary & hypothalamic failure
169
risk of emergency surgery with hypothyroidism
anaemia
bradycardia
hypotension
hypothermia
confusion
delayed anaesthetic recovery
170
