acute care Flashcards
NSAIDS side effects
NSAIDs
CVS – heart failure, stroke Resp - bronchospasm
GI – stomach ulcers
GU – renal failure
Opiods side effects
CNS – drowsiness, hallucinations Resp – respiratory depression (RR<8)
GI – nausea, constipation
GU – urinary retention
Derm – rash (due to histamine release)
Psych – tolerance, dependence, addiction
Naloxonethinking of infection - signs of infection
SLIPR
Swelling
Loss of function
Increased temperature (fever) Pain/ pus
Redness / rigors -> in hospital
Basal Cell Carcinoma
Clinical Features
Clinical Features
• Rolled edge
• Shiny/ pearly appearance • Telangiectasia
• Ulceration (rodent ulcer) • Non-healing
• Can be pigmented
Basal Cell Carcinoma
locations
• Typically present on face
Basal Cell Carcinoma RF
• Risk factors – elderly, UV exposure, immunosuppression, exposure to ionising radiation, arsenic exposure, Xeroderma pigmentosa
Basal Cell Carcinoma management
Management
• Topical agents – 5-fluorouracil and imiquimod • Cryo/radiotherapy
• Excision biopsy / Mohs micrographic surgery
Squamous Cell Carcinoma
RF
Risk factors
- Elderly
- Previous SCC or another skin cancer
- Precancerous (Actinic/solar keratosis & Bowen’s disease
- Outdoor occupation (Sun exposure)
- Fair skin
- Previous cutaneous injury
- Ulcers (Marjolin’s ulcer)
- Inherited conditions (Xeroderma Pigmentosum & albinism)
- Immunosupression
Squamous Cell Carcinoma
Clinical features
Clinical features • Enlarging scaly/crusted lesion • May ulcerate • Grows over weeks to months • Often painful • Located on sun exposed sites
Squamous Cell Carcinoma
Management
Treatment
• Nearly always treated surgical (either excision biopsy or Mohs micrographic surgery)
• Cryotherapy (for very small/low risk) /Radiotherapy (adjuvant/not fit for surgery)
referral for BCC and SCC
Early referral to dermatologist as 2 week wait for SCC/ routine referral for BCC
Causes of CKD
– Diabetes – Hypertension – Glomerulonephritis – Cystic kidney disease – Autoimmune disease (SLE/anti-GBM/vasculitis) – Obstruction/stone disease – Recurrent UTIs – Renovascular disease – Congenital (Alport’s)
Management of CKD:
3 main principles
– Treat the underlying cause e.g immunosuppression
– Prevent progression
• BP and glycaemic control, RAS inhibition
– Manage complications
• Renal anaemia, bone health, managing CV risk, diet
• Fluid overload, uraemia, infection risk
• CKD is defined a
reduced kidney function (eGFR < 60ml/min per 1.73m2) for 3 or more months, irrespective of cause
Clinical Features of Coeliac Disease
Presentation commonest in infants and in 50’s
• Non-specific symptoms (e.g. tiredness, malaise)
• Anaemia
• Nutritional deficiency
• Increased incidence of atopy and autoimmune diseases
• Histology typically shows villous atrophy and crypt hyperplasia with lymphocytic infiltration
Coeliac Disease histology
Histology typically shows villous atrophy and crypt hyperplasia with lymphocytic infiltration
Investigations for Coeliac Disease
FBC shows anaemia (folate/iron deficiency)
• Tissue transglutaminase (tTG) antibodies positive
• Distal duodenal biopsy
• Dual Energy X-ray Absorptiometry (DEXA) – at diagnosis
Management of Coeliac Disease
• Gluten free diet (risk of intestinal T cell lymphoma)
cough acute subacute chronic timeframes
Acute: < 3 weeks
Subacute: 3-8 weeks Chronic: > 8 weeks
cough history
Most important 2 questions:
- How long have they had the cough?
- Is it productive or dry? Haemoptysis? ▪ Pattern to cough?
- Nocturnal (Asthma, GORD, UACS, pulmonary oedema)
- On exercise (asthma/cough variant asthma)
- Environments (asthma, hypersensitivity pneumonitis, UACS)
▪ Associated symptoms? - URTI symptoms
- Shortness of breath (et change, progression, pattern)
- Systemic sx: fevers (pneumonia, tb), night sweats or weight loss (lung ca, tb) - Pleuritic chest pain
- Heart burn or reflux
cough acute DDX
productive - Bronchitis
Pneumonia
dry - URTI
Asthma/COPD
Drug induced
Congestive heart failure Smoke/toxin inhalation
PE
Hypersensitivity pneumonitis Pericarditis
cough Subacute (3 – 8 weeks) ddx
productive -
Pneumonia
dry Post infectious Pertussis
cough investigations
Investigations
▪Anyone with red flag symptoms or persistent chronic cough need formal investigation ▪Spirometry (restrictive vs obstructive)
▪ CXR
▪If productive sputum mcs. RVS w/ PCR. ▪Bloods – FBC, CRP, LFTs, Renal profile. ▪CT Chest
▪BNP +- Echo
▪Manometry/OGD
▪Bronchoscopy
▪Bronchial provocation test
▪QuantiFERON-TB gold/ T-spot test, BD Glucan, galactomannan antigen test, Vasculitic screen, AI screen
Cushing’s Syndrome
causes
ACTH Dependent - pituitary tumour, small cell lung cancer, carcinoid tumour
ACTH Independent
Steroids
Adrenal adenoma
Adrenal Carcinoma
Cushing’s Syndrome presentation
Signs and symptoms: • Moon face • Buffalo hump • Truncal obesity • Thin skin/easy bruising/striae • Osteoporosis/fractures • Reduced inflammatory and immune response • Rhabdomyolysis • Vasoconstriction and water retention • Reduce GnRH
Cushings Investigations
Exclude exogenous causes! 24h urinary free cortisol level
Cushing’s syndrome possible if result is positive (>50 mcg/24h), need additional investigations. Test twice on separate days for diagnostic reliability.
Low dose dexamethasone suppression test (1mg)
Cushing’s syndrome likely if results positive (morning cortisol >1.8 mcg/dL) combined with positive 24h urinary free cortisol level. Rule out false positives.
High dose dexamethasone suppression test (8mg)
Cushing’s syndrome confirmed if positive (cortisol <50% of baseline) and suggests pituitary cause.
Plasma ACTH
Determine if etiology of Cushing’s syndrome is ACTH dependent or independent. Pituitary or ectopic cause if >20 picograms/mL. Adrenal cause if <5 picograms/mL
Pituitary MRI/Adrenal CT
Treatment bushings
Treat primary cause of Cushing’s Syndrome
Surgical treatment
• Transsphenoidal pituitary adenectomy
• Adrenalectomy
• Surgical resection of tumour
• +/- chemo/radiation therapy
Medical treatment
• Somatostatin analogue: Pasireotide
• Adrenal steroid inhibitors: Ketoconazole, Metyrapone
• Glucocorticoid receptor antagonist: Mifepristone
• Post-surgical/radiation corticosteroid replacement therapy
phaeochromocytoma is a rare catecholamine secreting tumour.
clinical features
Features are typically episodic hypertension (around 90% of cases, may be sustained) headaches palpitations sweating anxiety
Phaeochromocytoma investigatios
Tests
24 hr urinary collection of metanephrines (sensitivity 97%*)
this has replaced a 24 hr urinary collection of catecholamines (sensitivity 86%)
Phaeochromocytoma management
Surgery is the definitive management. The patient must first however be stabilized with medical management:
alpha-blocker (e.g. phenoxybenzamine), given before a
beta-blocker (e.g. propranolol)
seizure history
Surgery is the definitive management. The patient must first however be stabilized with medical management:
alpha-blocker (e.g. phenoxybenzamine), given before a
beta-blocker (e.g. propranolol)
Status Epilepticus
management
Management (NICE) Stage 1 - 0-10mins: • Secure airway • High flow O2 • Assess A-E • IV access if possible • First dose of benzodiazepine (PR diazepam/IV lorazepam)
Stage 2 (11-29mins) • Regular observations • Repeat benzo dose if indicated
Stage 3 - Established Status Epilepticus (30- 60mins)
• Phenytoin and/or phenobarbital infusion
• Call anaesthetics/ITU –> ?intubation
Traumatic Brain Injury patient in ER Resuscitation and evaluation
ABCDE (ATLS guideline) > Special attention to hypoxia and hypotension.
GCS 8 or less > involve anesthetist or critical care physician to provide appropriate airway management.
Clotting function should be checked and corrected.
Traumatic Brain Injury patient in ER
Primary investigation of choice
: CT imaging of the head
Head injury
Indications of CT imaging within 1 hour:
Indications of CT imaging within 1 hour:
- CGS <14 at any point.
- GCS <15 at 2 hours.
- Focal neurological deficits.
- Suspected open, depressed or basal skull fracture.
- More than one episode of vomiting.
- Post-traumatic seizure.
Head injury
Indications within 8 hours:
Indications within 8 hours:
- Age >65
- Coagulopathy (aspirin, warfarin or rivaroxaban use) - Dangerous mechanism of injury (fall from hight, RTA) - Retrograde amnesia >30 minutes.
Cardinal signs of brain compression and herniation
1) Contralateral hemiparesis (compression of corticospinal tract in midbrain)
2) Decreasing GCS (involving reticular system)
3) Ipsilateral pupillary dilatation (compressed parasympathetic fiber of oculomotor nerve at tentorial hiatus)
Causes of Delirium - PINCHME
Pain (or pain-killers – opioids in AKI), palliative, post-surgical, trauma/bleed*
• Infection (UTI, Chest infection, Cellulitis or Sepsis), isolation
• Nutrition, Night pattern (sleep cycle), Noise (too quiet/loud)
• Constipation, Continence (new change)
• Hydration status, hyper(metabolic/endocrine), hypo(metabolic/endocrine/ fluid/electrolyte imbalance), hallucinations
• Medication (polypharmacy/concordance/ substance abuse*), mobility
• Environment (over/under stimulation), Emotional (stressors)
delirium Investigations
- History – collateral Hx
- Examination - thorough
- FBC, U+Es, LFTs, CRP
- Glucose
- TFTs
- Magnesium, Calcium Phosphate
- B12, folate, iron studies
- ABG if desaturating
- CXR
- MSU (DO NOT DO URINE DIP AS A POSTIVIE DIP DOES NOT MEAN THAT THEY HAVE AN INFECTION)
- ECG
Management of Delirium
• Effective communication and • re-orientation • Reassurance by involving family and friends • Stable environment • 1:1 nursing if at risk of falls
Treat underlying cause
• Stop medications
• Reduce Anticholinergics
• Sedate with lorazepam – 1- 2mg at night (IM/Oral) – peak effect 90mins
• Optimise visual and auditory • acuity
• Non-verbal communication
• Do not argue or correct
delusions
• Temporary physical restraints
In dementia, can give olanzapine 2.5mg ON (max dose 10mg), alternatively can give risperidone (increases cardiac/stroke events)
• Haloperidol 0.5mg-1mg is the last resort
MMSE
As per NICE : • Normal 25 or more • Mild Impairment 21-24 • Moderate Impairment 10-20 • Severe Impairment <10
dementia investigation
Cognitive tests: MMSE (≤23/30), Addenbrookes (ACE), MoCA Bloods: FBC, U+Es, TFTs, B12/folate, Ca2+
Imaging: CT, MRI, functional neuroimaging
Biochemical features of HypoPT
hypocalcemia
hyperphosphatemia
low or inappropriately normal levels of parathyroid hormone (PTH)
hypercalciuria
hypernaterium causes
Hypovolaemic Renal loss of Na urine Na >20 mmol/day Diuretic use Salt wasting nephropathy Mineralocorticoid deficiency/adrenal insufficiency Renal tubular acidosis Extrarenal(renal conservation ) urine Na <20 mmol/day Burns Gastrointestinal loss Pancreatitis Blood loss
Euvolaemic : Thiazide diuretics (can be euvolaemic or hypovolaemic) Hypothyroidism Adrenal insufficiency (can be euvolaemic or hypovolaemic) SIADH
Hypervolaemic
Congestive cardiac failure Cirrhosis
Nephrotic syndrome
Syndrome of Inappropriate Anti Hormone secretion (SIADH)
criteria
Essential criteria –Rule of 3
◦ osmolality –Urine > 100 & serum < 275 mOsm/kg
◦ Urine Na 30 mmol/l
◦ No other causes -Absence of adrenal, thyroid, pituitary or renal insufficiency, Diuretics
Causes of SIADH
Malignant disease Bronchogenic carcinoma Pulmonary disorders Viral and bacterial pneumonias Tuberculosis Neurologic disorders Encephalitis Meningitis Trauma Stroke Alcohol withdrawal Other HIV/AIDS Acute psychosis Acute intermittent porphyria Idiopathic
Primary Polydipsia
Psychiatric disorder, often complicated by increased thirst with antipsychotic meds
can occur with hypothalemic lesions (sarcoid or other infiltrative processes)
Usually no hyponatremia unless intake over 10-15 L/day, or acute 3-4 L water load
Urine osm below 100 (NOT ADH problem!)
Increased problems if other ADH stimulus (n/v, anxiety)
Treatment hyponatremia
Fluid restriction – 1 L per day or less
Hypertonic saline – If severe
Medications
◦ Demeclocycline –( a tetracycline derivative) - inhibits cyclic AMP, which diminishes the intracellular effects of ADH on the renal tubular cells
◦ Vaptans - vasopressin-2 receptor antagonists – (Tolvaptans )
Produces selective diuresis ( Aquaresis) with no effect on K & Na
total anterior circulation stroke
ALL THREE
unilateral weakness of face, arm and leg
homonymous hemiopoea
higher cerebral dysfunction
Partial anterior circulation stroke
two or more of
unilateral weakness of face, arm and leg
homonymous hemiopoea
higher cerebral dysfunction
lacunar stroke
one of
pure sensory stroke
pure motor stroke
ataxic hemiparseis
post thromblysis care
monitor - GCS, pulse and BP every 15 mins for 2 hours and then 30 mins for next 6
after if no haemorrhage start aspirin 300mg
stroke not in anticoagulant window
300 mg once daily for 14 days, before being considered for anticoagulant treatment.
post stroke clopidogrel not tolerated
If clopidogrel is contraindicated or not tolerated, given aspirin and modified release dipyramidole for secondary prevention following stroke
Barthel index
The Barthel index is a scale that measures disability or dependence in activities of daily living in stroke patients
standard target time for thrombectomy
The standard target time for thrombectomy in acute ischaemic stroke is 6 hours
‘Young’ stroke blood tests
thrombophilia and autoimmune screening - performed in those under 55 with no obvious cause of a stroke
Anterior cerebral artery
Contralateral hemiparesis and sensory loss, lower extremity > upper
Middle cerebral artery
Contralateral hemiparesis and sensory loss, upper extremity > lower
Contralateral homonymous hemianopia
Aphasia
Posterior cerebral artery
Contralateral homonymous hemianopia with macular sparing
Visual agnosia
Weber’s syndrome (branches of the posterior cerebral artery that supply the midbrain)
Ipsilateral CN III palsy
Contralateral weakness of upper and lower extremity
Posterior inferior cerebellar artery (lateral medullary syndrome, Wallenberg syndrome)
Ipsilateral: facial pain and temperature loss
Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus
• Murphy sign
in acute cholecystitis pain is experienced by the patient on inspiration (liver & gall bladder pushed downward) when an examiner’s hand is pressed towards the right upper quadrant due to the inflammed gall bladder hitting the examining hand.
Boas sign
in acute cholecystitis there is an area of hyperaesthesia between 9th - 11th ribs below the tip of right scapula elicited by stroking the skin in that area.
Rovsing sign
in acute appendicitis palpation of the left iliac fossa causes pain the the right iliac fossa.
Grey Turner’s sign
Flank bruising due to blood tracking into the
retroperitoneal plane from haemorrhagic pancreatitis or rupture of abdominal or iliac aneurysm.
Cullen’s sign
Periumbilical bruising due to haemorrhagic pancreatitis,
ruptured ectopic pregnancy r other causes of haemoperitoneum.
Intestinal obstruction presentations
Vomiting (early in small bowel obstruction cf large bowel obstruction) • Vomiting of food – obstruction above 2nd part of duodenum
• Vomiting of bile – obstruction below 2nd part of duodenum
• Abdominal pain - colicky
• Abdominal distension
• Absolute constipation – unable to pass flatus or motions
can be mechanical or adynamic
Features of strangulation in obstruction
Mechanical obstruction symptoms sudden & pronounced
• Continuous pain or dull ache between colic
• Localised to region of affected bowel
• Localised tenderness
• Guarding, no bowel sounds, tachycardia
General post-operative complications
- Nausea
- Hiccups
- Headaches
Post–op pulmonary complica
Pulmonary collapse • Pulmonary infec9on • Respiratory failure • ARDS • Pleural effusion • Pneumothorax • Stop smoking pre-op
Post-op cardiac complications
Myocardiac ischaemia /infarction • Cardiac failure • Arrhythmias • Post-operative shock • Management • Exclude surgical complications as causes
Post-op thromboembolism
- DVT
- Anti-thromboembolism measures • TED stockings
- Subcutaneous heparin
- Intra-operative calf-pumps
- Pulmonary embolism
- History of DVT
- Hip operations
- Anti-thrombin III deficicency; Protein S def; Protein C def
Post-op urinary complications
Urinary retenFon
• Post hernia repair, anorectal surgery, prostaFsm • UTI
• Urinary catheter, urethral instrumentaFons
• Renal failure
• Fluid/blood loss, jaundice (hepatorenal syndrome),
hypotension/shock, nephrotoxic drugs
Post-op cerebral complica9ons
- CVA
- Neuropsychiatric complications • Delirium tremens
- Post TURP syndrome
Post-op pyrexia
At 1-2 days • Physiologicalresponsetosurgery • Pulmonarycollapse,atelectasis At 3-5 days • Woundinfection • Intra-abdominalcollection • Chestinfection • Catheter/centrallinerelatedinfection At 5-7 days • Anastomoticdehiscence,DVT After 7 days • Sepsis–intra-abdominalcollection/othersources
Hartmann’s procedure
Indications
Resect pathology in sigmoid colon: end colostomy and closure of rectal stump • DiverIcular inflammatory mass / abscess / fistula • DiverIcular perforaIon • DiverIcular haemorrhage • Sigmoid carcinoma • ObstrucIon • PerforaIon • Sigmoid volvulus • ColiIs • Massive colonic haemorrhage
Splenectomy: complica?ons
- Post-op
- Bleeding
- Pancreatic injury
- Pulmonary complications • Thrombotic complications • Subphrenic abscess
- Late
- Overwhelming sepsis
- Prophylactic antibiotics
Laparoscopic cholecystectomy
Early complications • Bleeding • Bile leak • Damage to common bile duct Late complications • Retained stones • Bile duct stricture
Nissen fundoplication
for GORD
ost-op complications • Too tight a fundoplication
• Unable to burp / vomit • Recurrence of reflux
Gastrectomy complications
•
Gastrectomy complications • Early • Anastomotic leak • Bleeding • Delayed gastric emptying • Late • Iron def anaemia • B12 deficiency • Hypocalcaemia • Carcinoma
Dumping syndrome - Osmotic effect due large amount of food enters into the jejunum
Right hemicolectomy
remove the right-hand portion of the colon (approximately half the colon). This will include the caecum, ascending colon and a portion of the transverse colon.
Left hemicolectomy
the descending colon is removed. This is the part of your colon that’s attached to your rectum. After it’s removed, the surgeon attaches the transverse colon directly to your rectum
Ileopouch anal anastomosis IPAA indications
Ulcerative colitis
• Familial adenomatous polyposis coli (FAP)
Stomas
Ileostomies
• Loop
• End
Colostomies
• Loop
• End
• Double barrel
Ileostomies
loop = loop ileostomy is typically temporary and performed to protect a surgical join in the bowel.
End - large bowel (colon) is removed-and the end of your small bowel is brought to the surface of the abdomen to form a stoma. (if permanent - Ulcerative colitis or familial adenomatous polyposis)
They are typically located in the right iliac fossa (RIF).
Less water is absorbed in the small bowel so the contents of the stoma bag tend to have a liquid consistency.
Because the enzymes contained in small bowel contents can irritate the skin, the bowel has a spout sticking out from the abdominal wall. This allows faeces to drain without touching the skin.
colostomies - made using the large bowel (or colon).
flush to the skin (i.e. no spout) because the enzymes present in large bowel contents are less alkali and therefore less irritating to the skin.
main risk factor for cholangiocarcinoma
PSC
Epididymal cysts
Features
separate from the body of the testicle
found posterior to the testicle
Associated conditions
polycystic kidney disease
cystic fibrosis
von Hippel-Lindau syndrome
Diagnosis may be confirmed by ultrasound
preferred diagnostic test for chronic pancreatitis
CT pancreas with IV contrast
Postoperative ileus
Disruption of the normal coordinated movement of the GI tract following (abdominal or non abdominal) surgery
Physiological post op ileus – generally benign, self-resolving (0-72h)
Prolonged – suggested ileus >5d abnormal (40% of patients following laparotomy)
Aetiological inf lammatory, pharmacological (opioids), hormonal (stress response)
Abdo pain, bloating, nausea and vomiting, may or may not continue to pass flatus and stool
Management: NG tube for decompression if required, iv fluids, slowly introduce oral intake (chewing gum/sweets), correct electrolyte imbalances, early mobilisation and wean off opioids
incisional hernia management
Surgical repair with mesh
Recurrence - up to 50% of large hernias
or conservative - think of patient health and wellbeing
four cardinal features of intestinal obstruction:
Vomiting (faeculent)
Colicky pain (tinkling bowel sounds) Constipation
Abdominal distension
Small v large bowel obstruction:
Small bowel obstruction Vomiting occurs earlier Distension less Pain higher in abdomen Absolute constipation less likely Large bowel obstruction Vomiting occurs later Distension more Pain lower in abdomen Absolute constipation more likely
Ileus v mechanical obstruction
Ileus
No pain
Tinkling bowel sounds absent
Obstruction
Pain
Tinkling bowel sounds present
Simple/closed loop/strangulated obstruction
Simple-one obstructing point with no vascular compromise
Closed loop-obstruction present at two points, forming a loop of grossly distended bowel at risk of perforation
Strangulated-Blood supply compromised. Peritonism the cardinal feature.
General principles of management of obstruction
mmediate action: NBM, NGT, IV fluids, correct electrolyte imbalance, analgesia, AXR, CXR, bloods
Further imaging:
Colonoscopy in instances of suspected mechanical obstruction
Water soluble contrast (diagnostic and therapeutic)
Surgery:
Dependent on multiple factors. Strangulation/closed loop obstruction and large bowel often require surgery
Caecal volvulus
Investigations: AXR, contrast enema, CT Treatment:
Colonoscopic decompression (if unfit for surgery) Reduction alone
Right hemicolectomy
Caecostomy
Caecopexy
78yo F c/o PR bleed with associated dizziness & abdo pain…DDX
Haemorroids fissure polyps colitlis carcinoma Angiodysplasia
Management of acute LGI bleed
. ABC resuscitation
2. History & examination
3. IV access with 2x large bore cannulae & take bloods for FBC, clotting, renal function, crossmatch >2-4units
4. Fluid management – commence IV fluids (consider transfusion), monitor UO via catheter
5. Regular obs & commence stool chart
6. If bleed is persistent, massive &/or progressive then
consider urgent angiogram or surgery
7. Identify site & cause of bleeding for further management
PE presentation
Sudden-onset shortness of breath, pleuritic chest pain, and haemoptysis (this is the ‘typical’ triad, although note that all three features are rarely present).
A massive pulmonary embolism may present with the above and syncope/shock.
A small pulmonary embolism may be asymptomatic.
ECG PE
ECG finginds
ECG: Normal or sinus tachycardia. In a massive PE there may be evidence of right-heart strain (with P pulmonale, right axis deviation, right bundle branch block, and non-specific ST/T wave changes). The classic S1Q3T3 (deep S waves in lead I, pathological Q waves in lead III, and inverted T waves in lead III) is relatively uncommon (<20% of patients).
Exudative pleural effusions causes (think increase capillary permeability)
Exudative pleural effusions - Infections such as pneumonia or TB.
Malignancy such as bronchial carcinoma, mesothelioma, or lung metastases.
Inflammatory conditions such as rheumatoid arthritis, lupus, or acute pancreatitis.
Pulmonary infarct (for example secondary to a pulmonary embolism) and trauma.
Transudative pleural effusions (imbalances in the Starling forces that govern the formation of interstitial fluid.)
Conditions that increase the capillary hydrostatic pressure (forcing fluid out of the pulmonary capillaries into the pleural space) include congestive cardiac failure.
Conditions that reduce the capillary oncotic pressure (impairing the reabsorption of fluid from the pleural space into the pulmonary capillaries) include cirrhosis, nephrotic syndrome/chronic kidney disease, and gastrointestinal malabsorption/malnutrition (eg. Coeliac disease).
scardiodiss management
Management
Bilateral hilar lymphadenopthy alone - usually self-limiting
Acute sarcoidosis - bed rest, NSAIDs
Steroid treatment: oral or IV, depending on severity of disease
Immunosuppressants: in severe disease
Churg-Strauss Syndrome
mimic of asthma
granulomatous vasculitis associated with adult-onset asthma and eosinophilia.
Patients are pANCA +ve and have raised IgE levels. Treatment includes steroids and immunological agents in treatment-resistant cases such as Rituximab.
Pharmacological management of COPD involves:
- Short acting B2 agonist (SABA)/ short acting muscarinic antagonist (SAMA)
- with asthmatic features = acting B2 agonist (LABA) and inhaled corticosteroid in combination (ICS).
- w/o asthmatic features = long acting B2 agonist (LABA) AND a long acting muscarinic antagonist (LAMA).
- LAMA + LABA + ICS
- f patients are still symptomatic consider specialist referral.
The differential diagnoses for a lung nodule on chest x-ray include:
Malignancy which could be primary or secondary Foreign Body Abscess Cyst Granuloma Pulmonary hamartoma Arterio-venous malformation Carcinoid tumour Skin tumour
Non-pulmonary signs of sarcoidosis can be classified as follows:
Haematological features include bilateral parotid swelling, lymphadenopathy, and hepatosplenomegaly.
Ophthalmological features include anterior uveitis (causing a painful red eye) and keratoconjunctivitis sicca (dry eye).
Cardiovascular features include restrictive cardiomyopathy, pericarditis, and conduction defects.
Neurological features include cranial neuropathies (e.g. bilateral facial nerve palsy), peripheral neuropathy, myopathy, aseptic meningitis, transverse myelitis, and pituitary infiltration.
Renal features include renal stones (secondary to hypercalcaemia), nephrocalcinosis, and nephrogenic diabetes insipidus (secondary to hypercalcaemia).
Dermatological features include erythema nodosum (tender erythematous nodules on the shins) and lupus pernio (indurated purple plaques on the face).
calculate the CURB-65
C – confusion: An abbreviated mental test of ≤8
U – urea: >7mmol/L
R - Respiratory rate: ≥30/ min
B - blood pressure <90 systolic and/ or <60mmHg diastolic
65 - age: >65year old
Paraneoplastic Syndromes in Lung Cancer
Neurological
Polyneuropathy (Antibodies against the myelin sheath)
Cerebellar degeneration
Lambert-Eaton Syndrome
HPOA (Hypertrophic pulmonary osteoarthropathy) this occurs in 3% of cases. There will be joint stiffness, and severe pain in the wrists and ankles, sometimes also gynaecomastia. On x-ray there will be proliferative periostitis at the ends of the long bones, which have an ‘onion skin’ appearance. This is also associated with finger clubbing where cancer is the cause. It is thought to be caused by a blood borne factor released by the tumour – when patients have the primary tumour removed, the pain goes away!
Carcinoid syndrome - This presents with hepatomegaly, flushing and diarrhea
Inappropriate ADH secretion – this can cause hyponatraemia
Ectopic ACTH secretion – causing Cushing’s syndrome
Hypercalcemia (squamous) – due to the secretion of parathyroid hormone related peptides (PTHrp).
Lambert-Eaton Syndrome
autoantibody to presynaptic calcium channel on motor neurons
Symptoms/physical exam proximal muscle weakness difficulty rising from a chair difficulty climbing stairs ↓ tendon reflexes autonomic symptoms dry mouth impotence improves temporarily with muscle use (vs myasthenia gravis, where symptoms worsen with muscle use) spares extraocular muscles
Klebsiella Pneumonia
= Gram negative anaerobic rod-shaped bacteria
paracetamol OD management
If ingestion less than 1 hour ago + dose >150mg/kg: Activated charcoal
If staggered overdose or ingestion >15 hours ago: Start N-acetylcysteine immediately
If ingestion <4 hours ago: Wait until 4 hours to take a level and treat with N-acetylcysteine based on level
If ingestion 4-15 hours ago: Take immediate level and treat based on level
Obtain following bloods:
FBC
Urea and Electrolytes
INR
Venous gas
Consider need for transfer to liver unit if blood tests are worsening
Contraindications to thrombolysis in MI can be remembered using the mnemonic AGAINST:
Aortic Dissection GI bleed Allergic reaction Iatrogenic: recent surgery Neurological disease: recent stroke (within 3 months), malignancy Severe HTN (>200/120) Trauma, including recent CPR
Cautions and contra-indications to the use of Adenosine
IV Adenosine 3mg should not be administered to heart transplant patients, those who have central line access, or patients on medications that can potentiate the effects of Adenosine such as Dipyridamole or Carbamazepine.
Asthma is a contra-indication to the use of Adenosine so Verapamil should be used instead.
DKA management 1st hour
Management Hour 1
ABCDE assessment of the patient + large bore IV access
Arrange relevant investigations (they should not delay treatment)
1L 0.9% saline over 1 hour
Give STAT fluid challenge if systolic BP <90mmHg
Fixed rate insulin infusion (0.1 units/kg/hr) AFTER commencing fluid
Continue any long acting insulin the patient is already on
Initiate hourly:
Blood/capillary glucose
Blood/capillary ketones
Observations including GCS
Continuous ECG monitoring
DKA management 2-12
Continue fluid resuscitation (with potassium if serum K<5.5mmol/L - check before every bag):
1L 0.9% saline + 40mmol KCl over 2 hours then
1L 0.9% saline + 40mmol KCl over 2 hours again then
1L 0.9% saline + 40mmol KCl over 4 hours then
1L 0.9% saline + 40mmol KCl over 4 hours again then
1L 0.9% saline + 40mmol KCl over 6 hours
Ensure falling ketones (at least 0.5mmol/L/hour)
Increase insulin rate if not achieved
Consider catheter to measure output (aim at least 0.5ml/kg/hour)
If capillary glucose falls below 14mmol/L start 125ml/hour 10% glucose alongside the saline
Continue fixed rate insulin until:
Blood ketones <0.3mmol/L AND
pH >7.3 AND
Bicarbonate >18mmol/L
Emergency Management of acute angle closure glaucoma
administering IV Acetazolamide and a topical beta-blocker such as Timolol. Muscarinic agonists such as pilocarpine eye drops may be given. An urgent Ophthalmology referral should be made.
The definitive management for this condition is a peripheral iridotomy to relief the intraocular pressure.
empirical treatment for suspected encephalitis
IV aciclovir and IV ceftriaxone to cover for bacterial infections.
Treatment of hypoglycaemia depends on the severity:
Mild (i.e. still conscious)
Eat/drink 15-20g fast acting carbohydrate such as glucose tablets, a small can of Coca-Cola, sweets or fruit juice.
AVOID chocolate
Eat some slower acting carbohydrate afterwards (e.g. toast)
Severe (e.g. unconscious, seizing)
200ml 10% dextrose IV
1mg/kg glucagon IM if no IV access (will not work if caused by acute alcohol because of its action in blocking gluconeogenesis)
Treat seizure if prolonged or repeated
Aftercare
Consider medication changes
Investigate non-drug causes if necessary
management of HHS
Management
Fluid resuscitation
Fluid of choice is 0.9% saline:
1L over 1-2 hours
1L (+KCl) over 2-4 hours
1L (+KCl) over 4-6 hours
1L (+KCl) over 6-8 hours
1L (+KCl) over 8-10 hours
Patients may require subsequent fluid to correct dehydration
Change to 0.45% saline only if failing to reduce osmolality by approx. 5mOsm/kg/hour
Insulin at 0.05 units/kg/hour
Only if ketones >1mmol/L or glucose fails to fall
Continue any long acting insulin
VTE prophylaxis - these patients are high risk due to dehydration
Myxoedema coma
severe hypothyroidism leading to decreased mental status, hypothermia, and other symptoms related to slowing of function in multiple organs.
Management of myxoedema coma involves the following:
ITU/HDU care as required IV T3/T4 50-100mg IV hydrocortisone Mechanical ventilation and oxygen - if hypoventilation IV fluid - to correct hypovolaemia Correct hypothermia Correct hypoglycaemia Treat any heart failure
Thyrotoxic storm,
Symptoms of a thyrotoxic storm include:
high blood pressure
high temperature
tachycardia
Management
Management of thyrotoxic storm involves the following steps:
Symptom control:
IV propanolol
IV digoxin if propanolol fails or is contraindicated (e.g. asthma, low BP)
Reduce thyroid activity:
Propylthiouracil - preferred because it inhibits peripheral thyroxine conversion
Lugol’s iodine 4 hours later
Methimazole/carbimazole is considered second-line
IV hydrocortisone to reduce thyroid inflammation
Treat complications: (e.g. heart failure, hyperthermia)
Addisonian Crisis
low blood pressure, low blood levels of sugar and high blood levels of potassium.
Management of Addisonian Crisis
Management includes:
Fluid resuscitation is hypotensive.
IV hydrocortisone 100mg
IV glucose if hypoglycaemic
Swap back to their oral steroids after 3 days
Consider fludrocortisone if there is adrenal disease
Complications
Complications of Addisonian Crisis include:
Low blood pressure Vomiting and diarrhoea Dehydration Shock Coma Death
phaeochromocytoma - Acute management
Acute management
Management of phaeochromocytoma involves controlling the side-effects of excess adrenaline production:
Phentolamine IV (short acting alpha blocker) - to initially control BP
Phenoxybenzamine (longer acting alpha blocker) - to control BP before surgery can be arranged
Labetolol (beta blocker) - can be used if patient has tachyarrhythmia but only AFTER alpha blockade
Definitive management
Adrenalectomy can be performed 4-6 weeks after blood pressure is controlled.
Diagnosis of Peptic Ulcers
Diagnosis is confirmed using oesophago-gastro-duodenoscopy (OGD)
Management of non-variceal bleeding
ABCDE IV access IV fluids Catherine Urgent endoscopy
Bradycardia is defined as a heart rate < 60
Management with adverse feature
edical therapy should be started immediately if there is evidence of haemodynamiccompromise, regardless of the cause, and continued until temporary cardiac pacing is initiated.
The most common medications used to increase ventricular rate are intravenous atropine, epinephrine (adrenaline), and dopamine.
Patients who are not responsive to medical therapy require prompt temporary pacing. The two most commonly used modes of temporary pacing are transcutaneous and transvenous.
acute bronchitis management
dvise the person on self-care strategies such as adequate fluid intake, and the use of paracetamol or ibuprofen for symptomatic relief.
Do not routinely offer an antibiotic to treat an acute cough associated with acute bronchitis in people who are not systemically very unwell or at higher risk of complications. Inform the person that:
Acute bronchitis is usually a self-limiting illness and the cough usually lasts about three to four weeks.
Antibiotics do not make a large difference to the duration of symptoms, only shortening cough duration by about half a day on average.
Adverse effects, including diarrhoea and nausea are possible with antibiotic treatment.
Unnecessary antibiotic prescriptions may result in antibiotic resistance.
f antibiotics are indicated, for adults 18 years of age and older:
First-line choice is oral doxycycline: 200 mg on the first day, then 100 mg once a day for 4 days (5-day course in total). Note doxycycline should not be given to pregnant women.
Cerebrovascular accident (CVA)
= stroke
Need urgent head CT to see if haemorrgic or ischmic
classical history of vestibular schwannoma
combination of vertigo, hearing loss, tinnitus and an absent corneal reflex
ARDS causes
Causes infection: sepsis, pneumonia massive blood transfusion trauma smoke inhalation acute pancreatitis cardio-pulmonary bypass
ARDS Clinical features
Clinical features are typically of an acute onset and severe: dyspnoea elevated respiratory rate bilateral lung crackles low oxygen saturations
(linked to acute pancretisis)
ARDS diagnosis of criteria
A chest x-ray and arterial blood gases are the key investigations.
Criteria (American-European Consensus Conference)
acute onset (within 1 week of a known risk factor)
pulmonary oedema: bilateral infiltrates on chest x-ray (‘not fully explained by effusions, lobar/lung collapse or nodules)
non-cardiogenic (pulmonary artery wedge pressure needed if doubt)
pO2/FiO2 < 40kPa (200 mmHg)
Acute tubular necrosis causes
There are two main causes of ATN; ischaemia and nephrotoxins:
ischaemia
shock
sepsis
nephrotoxins aminoglycosides myoglobin secondary to rhabdomyolysis radiocontrast agents lead
Features of tubular necrosis
Features
features of AKI: raised urea, creatinine, potassium
muddy brown casts in the urine
Histopathological of tubular necrosis
Histopathological features
tubular epithelium necrosis: loss of nuclei and detachment of tubular cells from the basement membrane
dilatation of the tubules may occur
necrotic cells obstruct the tubule lumen
Sterile pyuria and white cell casts in the setting of rash and fever
acute interstitial nephritis, which is commonly due to antibiotic therapy
Detect acute kidney injury, in line with the (p)RIFLE, AKIN or KDIGO definitions, by using any of the following criteria:
- a rise in serum creatinine of 26 micromol/litre or greater within 48 hours
- a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
- a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than
Should be stopped in AKI as may worsen renal function
- NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
- Aminoglycosides
- ACE inhibitors
- Angiotensin II receptor antagonists
- Diuretics
characteristics of thrombotic thrombocytic purpura (TTP):
Fever (T: 38ºC)
Altered mental state (headache, confusion, excess tiredness, seizure)
Thrombocytopenia (platelets: 130 * 109/L)
Haemolytic anaemia (haemoglobin: 98 g/L)
Reduced renal function (creatinine: 126 µmol/L)
Hypertension (this does not form part of the pentad of symptoms but may be present)
In type 1 diabetics, recommend monitoring blood glucose
at least 4 times a day, including before each meal and before bed
Causes of anaemia in renal failure
reduced erythropoietin levels - the most significant factor
reduced erythropoiesis due to toxic effects of uraemia on bone marrow
reduced absorption of iron
anorexia/nausea due to uraemia
reduced red cell survival (especially in haemodialysis)
blood loss due to capillary fragility and poor platelet function
stress ulceration leading to chronic blood loss
treat anaemia in renal failure
the 2011 NICE guidelines suggest a target haemoglobin of 10 - 12 g/dl
determination and optimisation of iron status should be carried out prior to the administration of erythropoiesis-stimulating agents (ESA). Many patients, especially those on haemodialysis, will require IV iron
ESAs such as erythropoietin and darbepoetin should be used in those ‘who are likely to benefit in terms of quality of life and physical function’
Autoimmune haemolytic anaemia (AIHA)
AIHA is characterised by a positive direct antiglobulin test (Coombs’ test)
Iron deficiency anaemia
low serum iron
High TIBC
Transferrin saturation low
low ferritin
Chronic disease anaemia
low serum iron
low TIBC
Transferrin saturation low
normal ferritin
Sideroblastic anaemia
It may be congenital or acquired
Congenital cause: delta-aminolevulinate synthase-2 deficiency
Acquired causes myelodysplasia alcohol lead anti-TB medications
Investigations
hypochromic microcytic anaemia (more so in congenital)
bone marrow: sideroblasts and increased iron stores
sickle crisis
Crisis management
analgesia e.g. opiates
rehydrate
oxygen
consider antibiotics if evidence of infection
blood transfusion
exchange transfusion: e.g. if neurological complications
Longer-term management
hydroxyurea
increases the HbF levels and is used in the prophylactic management of sickle cell anaemia to prevent painful episodes
NICE CKS suggest that sickle cell patients should receive the pneumococcal polysaccharide vaccine every 5 years
NICE use the following cut-offs to determine whether a woman should receive oral iron therapy:
Booking visit < 11 g/dl
28 weeks< 10.5 g/dl
Macrocytic anaemia
Megaloblastic causes
vitamin B12 deficiency
folate deficiency
Normoblastic causes alcohol liver disease hypothyroidism pregnancy reticulocytosis myelodysplasia drugs: cytotoxics
Causes of normocytic anaemia include
anaemia of chronic disease chronic kidney disease aplastic anaemia haemolytic anaemia acute blood loss
Causes of microcytic anaemia
iron-deficiency anaemia thalassaemia* congenital sideroblastic anaemia anaemia of chronic disease (more commonly a normocytic, normochromic picture) lead poisoning
normal haemoglobin level associated with a microcytosis
possibility of polycythaemia rubra vera which may cause an iron-deficiency secondary to bleeding.
Aplastic crises is characterised by
Aplastic crises is characterised by
reticulocytopaenia – seen after around 5 days post exposure and continues for 7 – 10 days
symptomatic anaemia
serum IgM antibodies to parvovirus B19 (1)
peripheral arterial disease management
As with any patient who has established cardiovascular disease, all patients should be taking a statin. Atorvastatin 80 mg is currently recommended. In 2010 NICE published guidance suggesting that clopidogrel should be used first-line in patients with peripheral arterial disease in preference to aspirin.
Exercise training has been shown to have significant benefits. NICE recommend a supervised exercise programme for all patients with peripheral arterial disease prior to other interventions.
Severe PAD or critical limb ischaemia may be treated by:
angioplasty
stenting
bypass surgery
Drugs licensed for use in peripheral arterial disease (PAD) include:
naftidrofuryl oxalate: vasodilator, sometimes used for patients with a poor quality of life
cilostazol: phosphodiesterase III inhibitor with both antiplatelet and vasodilator effects - not recommended by NICE
ankle-brachial pressure index (ABPI) of ? is diagnostic of critical limb ischia
An ankle-brachial pressure index (ABPI) of < 0.5 is suggestive of critical limb ischaemia.
Biliary colic is caused by gallstones passing through the biliary tree.
risk factors
it is traditional to refer to the ‘4 F’s’:
Fat: obesity is thought to be a risk factor due to enhanced cholesterol synthesis and secretion
Female: gallstones are 2-3 times more common in women. Oestrogen increases activity of HMG-CoA reductase
Fertile: pregnancy is a risk factor
Forty
other notable risk factors include:
diabetes mellitus
Crohn’s disease
rapid weight loss e.g. weight reduction surgery
drugs: fibrates, combined oral contraceptive pill
Biliary colic features
eatures
colicky right upper quadrant abdominal pain
worse postprandially, worse after fatty foods
the pain may radiate to the right shoulder/interscapular region
nausea and vomiting are common
Amyloidosis
Patients may present with features affecting multiple organs, such as:
The kidneys, with nephrotic syndrome/renal failure.
The gastrointestinal system, with macroglossia, malabsorption, or hepatosplenomegaly.
The neurological system, with neuropathies.
The vasculature, with periorbital purpura (racoon eyes).
Or the joints, with painful asymmetrical large joint inflammation.
Diagnosis
The diagnosis of amyloidosis requires tissue biopsy and apple-green birefringence when stained with Congo red and viewed under polarised light. Biopsy is often taken from the rectum (has sensitivity of 74–94%).
Basophilic stippling
megaloblastic anaemia, thalassaemias (in particular alpha thalassaemia), sideroblastic anaemia and alcohol abuse. A rare cause is the inherited disorder pyrimidine 5’-nucleotidase deficiency.
Howell Jolly Bodies
hyposplenism,
leukoerythroblastic film
marrow fibrosis or invasion, such as: primary myelofibrosis, metastatic cancer, TB and Gaucher’s dise
Acanthocytes or spur cells
The two most important causes are liver disease and neuroacanthocytosis (including abetalipoproteinemia and homozygous familial hypobetalipoproteinemia); but anorexia nervosa, hypothyroidism and myelodysplasia have also been associated.
Echinocytes or burr cells
Causes include: liver disease, vitamin E deficiency, end-stage renal disease, and the haemolytic enzyme disorder pyruvate kinase deficiency.
Disseminated intravascular coagulation (DIC) describes inappropriate activation of the clotting cascades, resulting in thrombus formation and depletion of clotting factors and platelets.
atients present with excess bleeding e.g. epistaxis, gingival bleeding, haematuria, bleeding from cannula sites. Patients may also present with fever, confusion, or coma.
This is often in the context of severe systemic disease
Physical signs include petechiae, brushing, confusion, and hypotension.
Risk factors od DIC
Risk factors
Major trauma or burns
Multiple-organ failure
Severe sepsis or infection.
Severe obstetric complications
Solid tumours or haematological malignancies
Acute promyelocytic leukemia (APL) is an uncommon subtype of acute myelogenous leukemia that is associated with DIC. This comes up frequently in written exams
Investigation findings in DIC
nvestigation findings
Thrombocytopenia
Increased prothrombin time
Increased fibrin degradation products (such as D-dimer)
Decreased fibrinogen
Essential thrombocytosis
50% of patients are asymptomatic, and diagnosed after an incidental blood test. The hallmark is an increased platelet count (>450 x 10^9/L).
JAK2 V617F mutation is present in 50-60% of patients with essential thrombocytosis, and helps distinguish essential thrombocytosis from secondary (reactive) thrombocytosis.
Thrombosis (arterial or venous)
Bleeding (gastrointestinal or intracranial)
Headache
Dizziness/syncope (secondary to hyper-viscosity).
Causes of pancytopaenia
Causes of pancytopaenia
Causes of decreased marrow haematopoetic function
Common causes include chemotherapy and radiotherapy (the pancytopenia may be transient).
Vitamin B12 and folate deficiency.
Marrow infiltration by haematological malignancies (leukaemias or lymphomas).
Myelofibrosis, in which there is progressive marrow fibrosis.
Multiple myeloma (a plasma cell dyscrasia).
Parvovirus infection in haemolytic disease (such as sickle cell anaemia).
Inherited causes of marrow failure
The most common causes include Fanconi’s anaemia (an autosomal recessive condition) and dyskeratosis congenita (an X-linked condition).
Increased destruction/sequestration of blood cells peripherally
This is seen in conditions affecting the liver (such as hepatitis B/C, autoimmune hepatitis, and cirrhosis).
Immune destruction of blood cells
This occurs in drug-induced pancytopenia (secondary to, for example, Sulphonamide or Rifampicin).
Haemolytic anaemia
low haemoglobin, high bilirubin (unconjugatd) and may be associated with reticulocytosis, raised LDH and raised urinary urobilinogen.
Myelofibrosis
Myelofibrosis is a myeloproliferative disorder of unknown cause, characterised by marrow fibrosis. It can present as a pancytopenia. It is more common in elderly patients (>65 years old).
Clinical features
Constitutional symptoms: weight loss, fever, night sweats
Splenomegaly: abdominal discomfort, early satiety
Marrow failure: anaemia, recurrent infection, and abnormal bleeding/bruising.
Hepatomegaly: seen in 50% of patients.
Diagnosis
On blood film, you would expect to see poikilocytes (tear-shaped red blood cells). Because of the marrow fibrosis, it is difficult to aspirate the bone marrow, resulting in a ‘dry tap’.
Associations of Non-Hodgkin’s Lymphoma
Helicobacter pylori with gastric MALT (mucosa-associated lymphoma tissue).
Epstein Barr virus with Burkitt’s lymphoma and AIDS-related CNS lymphoma.
Hepatitis C virus with diffuse large B-cell lymphoma and splenic marginal zone lymphoma.
Human T cell lymphotropic virus type 1 with T-cell lymphoma.
Post-splenectomy prophylaxis
Patients therefore require the following vaccinations:
Pneumococcal vaccination (with regular boosters every 5 years).
Seasonal influenza vaccination (yearly, typically every autumn).
Haemophilus influneza type B vaccination (one-off).
Meningitis C vaccination (one-off).
They recommend the following that we admit for intravenous antibiotics the following patients:in cellulitis
Has Eron Class III or Class IV cellulitis.
Has severe or rapidly deteriorating cellulitis (for example extensive areas of skin).
Is very young (under 1 year of age) or frail.
Is immunocompromized.
Has significant lymphoedema.
Has facial cellulitis (unless very mild) or periorbital cellulitis.
cellulitis management
Management
The BNF recommends flucloxacillin as first-line treatment for mild/moderate cellulitis. Clarithromycin, erythromycin (in pregnancy) or doxycyline is recommended in patients allergic to penicillin.
NICE recommend that patients severe cellulitis should be offered co-amoxiclav, cefuroxime, clindamycin or ceftriaxone.
venous ulceration management
Management
compression bandaging, usually four layer (only treatment shown to be of real benefit)
oral pentoxifylline, a peripheral vasodilator, improves healing rate
small evidence base supporting use of flavinoids
little evidence to suggest benefit from hydrocolloid dressings, topical growth factors, ultrasound therapy and intermittent pneumatic compression
Complications of cardiac catheterisation
Bleeding is the most common complication, secondary to arterial puncture. It is much less common in radial access versus femoral access. Pseudoaneurysm formation is a rare complication.
Arterial thrombosis causing occlusion of the radial or femoral artery can cause ischaemia of the distal limb. Loss of distal pulse can also be caused by arterial spasm.
Arrhythmias are often transient and include ventricular tachycardia and fibrillation (VF/VT), as well as atrial flutter. Bradycardia can also occur.
Perforation of the heart or great vessels leading to tamponade
Allergic reaction to iodine contrast or local anaesthetic
Atheroembolism - atheromatous debris can be scraped from the aortic wall, causing cerebral (Ischaemic stroke), retinal, renal or gastrointestinal emboli.
Indications for transcutaneous pacing in Bradyarrhythmias
Patients unresponsive to medical therapy (with e.g. atropine total dose 3 mg and adrenaline)
After an inferior myocardial infarction (unlike with anterior myocardial infarction, bradycardias are usually temporary and do not require permanent pacing)
Bradyarrhythmias requiring pacemakers
Complete heart block (whether asymptomatic or symptomatic)
Mobitz type 2 heart block (whether asymptomatic or symptomatic)
Symptomatic sick sinus syndrome
Permanent bradyarrhythmias caused by a myocardial infarct (typically anterior infarcts - arrhythmias caused by inferior infarcts tend to be temporary)
Inheritance of Hypertrophic cardiomyopathy
Inheritance is autosomal dominant, however half of cases are as a result of sporadic mutations where the parents do not carry a disease-causing mutation.
restrictive cardio myopathy causes
Familial non-infiltrative cardiomyopathy (inherited genetic disorders) Infiltrative: Amyloidosis Sarcoidosis Gaucher disease Hurler syndrome Fatty infiltration Storage: Haemochromatosis Fabry diseas Glycogen storage disorders Others: Diabetic cardiomyopathy Scleroderma Hypereosinophilic syndrome (Löffler's) Radiation
Surgical/device management options
Cardiac resynchronisation therapy
ICDs are indicated if the following criteria are fulfilled:
QRS interval <120ms, high risk sudden cardiac death, NYHA class I-III
QRS interval 120-149ms without LBBB, NYHA class I-III
QRS interval 120-149ms with LBBB, NYHA class I
infective endocarditis RF
Age > 60 years
Male sex
Intravenous drug use - predisposition to Staph. aureus infection and right-sided valve disease e.g. tricuspid endocarditis
Poor dentition and dental infections
Dukes Criteria for Infective Endocarditis
Major Dukes criteria
Blood culture positive for IE - two separate blood cultures (or Single positive blood culture for Coxiella burnetti or positive anti body titre)
Imaging positive for IE (Echocardiogram positive for IE)
Minor Dukes criteria
Predisposition e.g. predisposing heart condition or intravenous drug use
Fever > 38.0°C
Vascular phenomena e.g. arterial emboli, infarcts, mycotic aneurysms, intracranial or conjunctival haemorrhages, Janeway lesions
Immunological phenomena e.g. glomerulonephritis, Osler’s nodes, Roth’s spots, rheumatoid factor
Microbiological evidence e.g. blood culture not meeting major criteria, or serological evidence of active infection with organism consistent with IE
PR interval and IE
PR interval prolongation in a patient with Infective Endocarditis is an indication for surgery as it can be secondary to aortic root abscess
Non-shockable rhythms
Pulseless electrical activity: This is when there’s normal co-ordinated cardiac activity on the ECG monitor, but no pulse is present on the patient
Asystole: this refers to the absence of QRS complexes (or electrical activity) on the ECG leads.
Acute mitral regurgitation
cardiac emergency and may present with sudden onset pulmonary oedema, hypotension and cardiogenic shock.
cardiac emergency and may present with sudden onset pulmonary oedema, hypotension and cardiogenic shock.
Eradication of group-A beta-haemolytic streptococcal infection
STAT dose of IV Benzylpenicillin, with a ten day course of Phenoxymethylpenicillin to follow
Analgesia for arthritic symptoms
Aspirin or non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen or naproxen.
Aspirin should be used with caution in young children due to the small risk of Reye syndrome.
There is no evidence to suggest that NSAIDs help with outcomes related to carditis.
If carditis is complicated by heart failure
Glucocorticoids (e.g. Prednisolone) can provide benefit (NSAIDs should be stopped concurrently).
Diuretic treatment may also be necessary, and valve surgery if severe.
Sydenham’s chorea is self-limiting and does not require treatment, however Haloperidol or Diazepam may be used for distressing symptoms or risk of harm.
AAA screaning
In the UK, screening is offered at age 65 using abdominal ultrasound scan.
If small AAA (3-4.4cm) – offered yearly repeat ultrasound
If medium AAA (4.5-5.4cm) – offered repeat ultrasound every 3 months
If large AAA (>5.5cm) – surgery generally recommended.
acromegaly investigations
If a patient shows some of typical clinical features of acromegaly, it is recommended to measure IGF-1.
If IGF-1 is raised or equivocal, growth hormone is measured following intake of oral glucose (Oral Glucose Tolerance Test) to see if growth hormone is inappropriately suppressed and to confirm the diagnosis of acromegaly.
If acromegaly has been diagnosed, an MRI should be performed to assess the size and extent of the tumour. If MRI is contraindicated, CT scan is second line. If the tumour is found to be close to the optic chiasm, visual fields should be regularly tested.
features of adrenal insufficiency
Clinical Features
Hypotension
Fatigue and weakness
GI symptoms
Syncope
Pigmentation (due to an increase in ACTH pre-cursors).
Approximately 60% of patients with auto-immune Addison’s disease have vitiligo or other autoimmune endocrinopathies.
Management of Addisonian Crisis
The treatment is aggressive fluid rescuscitation and IV steroids.
Glucose is occasionally required if there is hypoglycaemia.
Amiodarone induced thyrotoxicosis
- TFT’s are completed as part of regular drug monitoring and that patients are made aware about the potential risks.
Treatment depends on the underlying type and may involve anti-inflammatories such as steroids plus anti-thyroid drugs (Carbimazole).
Close discussion with the Cardiology team is important to decide whether the Amiodarone needs to be stopped or substituted.
Abnormalities if thyroid function can occur in up to 50% of patients taking Amiodarone.
Metformin MOA
Increase peripheral insulin sensitivity and hepatic glucose uptake
Lactic acidosis and GI disturbance
Sulfonylureas
e.g. Gliclazide MOA
Depolarise islet cells in the pancreas increasing insulin release.
Hypoglycaemia and weight gain.
Thiazolidinediones
e.g. Pioglitazone MOA
Increase peripheral insulin sensitivity.
Fluid retention, weight gain and worsening heart failure.
SGLT2 Inhibitors MOA
e.g. Dapgliflozin
Increase urinary glucose loss.
Diabetic Ketoacidosis when used with insulin and increased risk of urinary tract infection
DPP4-Inhibitors
e.g. Sitagliptin
Inhibit GLP1 breakdown.
Hypoglycaemia and GI upset.
Causes of Cranial Diabetes Insipidus
Head trauma Inflammatory conditions e.g. sarcoidosis Cranial infections such as meningitis Vascular conditions such as sickle cell disease Rare genetic causes
Causes of Nephrogenic Diabetes Insipidus
Nephrogenic diabetes insipidus may be caused by:
Drugs e.g. lithium
Metabolic disturbances e.g. hypercalcaemia, hypokalaemia, hyperglycaemia
Chronic renal disease
Rare genetic causes (e.g. Wolfram’s syndrome).
Management of Cranial Diabetes Insipidus
Cranial diabetes insipidus can be managed with desmopression.
Sodium should be monitored routinely due to the risk of hyponatraemia.
Management of Nephrogenic Diabetes Insipidus
Nephrogenic diabetes insipidus is managed by correcting any metabolic abnormality and stopping any offending drugs.
High dose desmopressin has been used with variable results.
Other possible treatments include using a thiazide diuretic and a non-steroidal anti-inflammatory drug to reduce urine volume.
Management of erectile dysfucntion
Depends on cause Psychosexual therapy Oral phosphodiesterase inhibitors (Sildenafil) Vacuum aids Intra-cavernosal injections Prosthesis
Contraindications and cautions of Sildenafil
Contraindicated in: those taking nitrates, hypertension/hypotension, arrhythmias, unstable angina, stroke, recent myocardial infarction
Caution in: angina, peptic ulcer, liver or kidney impairment, Peyronie’s disease, complex antihypertensive regimes
Causes of Smooth Goitre
Graves' disease Hashimoto's disease Drugs (e.g. lithium, amiodarone) Iodine deficiency/excess De Quervain's thyroiditis (painful) Infiltration (e.g. sarcoid, haemochromatosis)
Causes of Nodular Goitre
Toxic solitary adenoma Non-functional thyroid adenoma Multinodular goitre Thyroid cyst Cancer
Combined HRT can be given either:
Cyclically: for peri-menopausal women who are still having menstrual periods
Continuous: for post-menopausal women who are not having menstrual periods
Biochemical Features of hyperaldosteronism
Hypertension
Hypokalaemia
Metabolic alkalosis
Pregnancy considerations in thyroid disease
Carbimazole – contraindicated in pregnancy
Propylthiouracil – Treatment of choice in first trimester pregnancy/thyroid storm
Management of Mild Hypoglycaemia (Still Conscious)
ABCDE
Eat/drink 15-20g fast acting carbohydrate such as glucose tablets, a small can of Coca-Cola, sweets or fruit juice.
AVOID chocolate
Eat some slower acting carbohydrate afterwards (e.g. toast)
Management of Severe Hypoglycaemia (eg. Seizures, Unconscious)
ABCDE 200ml 10% dextrose IV 1mg/kg glucagon IM if no IV access (will not work if caused by acute alcohol because of its action in blocking gluconeogenesis) Treat seizure if prolonged or repeated
Mointoring of hypotestoneroneism
assess for polycythaemia (testosterone has a direct effect on erythrocytosis)
bone mineral density (DEXA bone scanning, prostate status
LFT’s (synthetic hormones can affect liver function).
Gynaecomastia
impaired fasting glucose is a pre-diabetic state defined as:
Fasting glucose 6.1-7mmol/L
2h glucose <7.8mmol/L
Multiple Endocrine Neoplasia-1 (MEN-1) features
Caused by mutation in the MEN 1 gene
Parathyroid: hyperplasia/adenomas
Pancreas: gastrinoma, insulinoma
Pituitary: prolactinoma
Multiple Endocrine Neoplasia-2a (MEN-2a) features
Caused by mutation in the RET gene
Thyroid: medullary thyroid cancer
Adrenal: pheochromocytoma
Parathyroid: hyperplasia/adenomas
Amiodarone Side Effects
Hypothyroidism (more common than hyperthyroidism) Hyperthyroidism Corneal deposits Stevens-Johnson syndrome Grey discoloration of the skin Liver failure
Waterhouse-Friderichsen’s syndrome
severe bacterial infection which results in disseminated intravascular coagulation and subsequent adrenal haemorrhage and failure.
Pancreatitis (acute) features
autodigestion of pancreatic tissue by the pancreatic enzymes, leading to necrosis
Features:
severe epigastric pain that may radiate through to the back
vomiting is common
examination may reveal epigastric tenderness, ileus and low-grade fever
periumbilical discolouration (Cullen’s sign) and flank discolouration (Grey-Turner’s sign) is described but rare
Pancreatitis (acute) investigations
serum amylase
serum lipase
a diagnosis of acute pancreatits can be made without imaging if characteristic pain + amylase/lipase > 3 times normal level
however, early ultrasound imaging is important to assess the aetiology as this may affect management - e.g. patients with gallstones/biliary obstruction
other options include contrast-enhanced CT
Acute pancreatitis: management
fluid resuscitation
aggressive early hydration with crystalloids. In severe cases 3-6 litres of third space fluid loss may
NICE state the following: ‘Do not offer prophylactic antimicrobials to people with acute pancreatitis’
Chronic pancreatitis Features
inflammatory condition which can ultimately affect both the exocrine and endocrine functions of the pancreas.
Features
pain is typically worse 15 to 30 minutes following a meal
steatorrhoea: symptoms of pancreatic insufficiency usually develop between 5 and 25 years after the onset of pain
diabetes mellitus develops in the majority of patients. It typically occurs more than 20 years after symptom begin
Chronic pancreatitis investigations
Investigation
abdominal x-ray shows pancreatic calcification in 30% of cases
CT is more sensitive at detecting pancreatic calcification. Sensitivity is 80%, specificity is 85%
functional tests: faecal elastase may be used to assess exocrine function if imaging inconclusive
ascites SAAG > 11g/L
indicates portal hypertension
Liver disorders are the most common cause
cirrhosis/alcoholic liver disease
acute liver failure
liver metastases
Cardiac
right heart failure
constrictive pericarditis
Other causes Budd-Chiari syndrome portal vein thrombosis veno-occlusive disease myxoedema
ascites SAAG <11g/L
Hypoalbuminaemia
nephrotic syndrome
severe malnutrition (e.g. Kwashiorkor)
Malignancy
peritoneal carcinomatosis
Infections
tuberculous peritonitis
Other causes pancreatitisis bowel obstruction biliary ascites postoperative lymphatic leak serositis in connective tissue diseases
Management of ascites
reduce sodium
aldosterone antagonists: e.g. spironolactone
large-volume paracentesis for the treatment of ascites requires albumin ‘cover’. ( reduces paracentesis-induced circulatory dysfunction )
Offer prophylactic oral ciprofloxacin or norfloxacin for people with cirrhosis and ascites with an ascitic protein of 15 g/litre or less, until the ascites has resolved’
Acromioclavicular joint injury
during collision sports such as rugby following a fall on to the shoulder or a FOOSH (falls on outstretched hand).
Grade I and II injuries are very common and are typically managed conservatively including resting the joint using a sling.
Grade IV, V and VI are rare and require surgical intervention.
The management of grade III injuries is a matter of debate and often depends on individual circumstances.
Achilles tendinopathy (tendinitis) Features and management
Features
gradual onset of posterior heel pain that is worse following activity
morning pain and stiffness are common
The management is typically supportive
simple analgesia
reduction in precipitating activities
calf muscle eccentric exercises: this may be self-directed or under the guidance of physiotherapy
Achilles tendon rupture Imaging of choice
USS
hepatic LFT’s
Transaminitis: Aminotransferases (AST, ALT)
Generally associated with hepatocellular damage
AST: ALT =1
Associated with ischaemia (CCF and ischaemic necrosis and hepatitis)
AST: ALT >2.5
Associated with Alcoholic hepatitis
Alcohol induced deficiency of pyridoxal phosphate
AST: ALT <1
High rise in ALT specific for Hepatocellular damage
Paracetamol OD with hepatocellular necrosis
Viral hepatitis, ischaemic necrosis, toxic hepatitis
Autoimmune hepatitis Features
Features
may present with signs of chronic liver disease
acute hepatitis: fever, jaundice etc (only 25% present in this way)
amenorrhoea (common)
ANA/SMA/LKM1 antibodies, raised IgG levels
liver biopsy: inflammation extending beyond limiting plate ‘piecemeal necrosis’, bridging necrosis
Autoimmune hepatitis Management
Management
steroids, other immunosuppressants e.g. azathioprine
liver transplantation
Pre renal causes of AKI
ischaemia (ie. shock, stroke)
hypovolaemia secondary to diarrhoea/vomiting
renal artery stenosis
Intrinsic causes of AKI
toxins (drugs, contrast etc) or immune-mediated glomuleronephritis.
Examples glomerulonephritis acute tubular necrosis (ATN) acute interstitial nephritis (AIN), respectively rhabdomyolysis tumour lysis syndrome
Postrenal causes of AKI
think obstruction Examples kidney stone in ureter or bladder benign prostatic hyperplasia external compression of the ureter
Risk factors for AKI include:
chronic kidney disease
other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
history of acute kidney injury
use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics) within the past week
use of iodinated contrast agents within the past week
age 65 years or over
NICE recommend that we can use a variety of different criteria to make an official diagnosis of AKI. They state:
Detect acute kidney injury, in line with the (p)RIFLE, AKIN or KDIGO definitions, by using any of the following criteria:
a rise in serum creatinine of 26 micromol/litre or greater within 48 hours
a 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than
Drugs Should be stopped in AKI as may worsen renal function
- NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
- Aminoglycosides
- ACE inhibitors
- Angiotensin II receptor antagonists
- Diuretics
Drugs May have to be stopped in AKI as increased risk of toxicity (but doesn’t usually worsen AKI itself)
- Metformin
- Lithium
- Digoxin
hyperkalaemia - Stabilisation of the cardiac membrane
Intravenous calcium gluconate
hyperkalaemia Short-term shift in potassium from extracellular to intracellular fluid compartment
Combined insulin/dextrose infusion
• Nebulised salbutamol
hyperkalaemia Removal of potassium from the body
- Calcium resonium (orally or enema)
- Loop diuretics
- Dialysis
AKI Refer to a nephrologist if any of the following apply:
Renal tranplant ITU patient with unknown cause of AKI Vasculitis/ glomerulonephritis/ tubulointerstitial nephritis/ myeloma AKI with no known cause Inadequate response to treatment Complications of AKI Stage 3 AKI (see guideline for details) CKD stage 4 or 5 Qualify for renal replacement hyperkalaemia / metabolic acidosis/ complications of uraemia/ fluid overload (pulmonary oedema)
Epididymo-orchitis features
Features
unilateral testicular pain and swelling
urethral discharge may be present, but urethritis is often asymptomatic
factors suggesting testicular torsion include patients < 20 years, severe pain and an acute onset
Epididymo-orchitis Management
the British Association for Sexual Health and HIV (BASHH) produced guidelines in 2010
if the organism is unknown BASHH recommend: ceftriaxone 500mg intramuscularly single dose, plus doxycycline 100mg by mouth twice daily for 10-14 days
further investigations following treatment are recommended to exclude any underlying structural abnormalities
Testicular tumours features
If inguinoscrotal swelling; cannot ‘get above it’ on examination
Cough impulse may be present
May be reducible
Acute epididymo-orchitis
Often history of dysuria and urethral discharge
Swelling may be tender and eased by elevating testis
Most cases due to Chlamydia
Infections with other gram negative organisms may be associated with underlying structural abnormality
Epidiymal cysts
Single or multiple cysts
May contain clear or opalescent fluid (spermatoceles)
Usually occur over 40 years of age
Painless
Lie above and behind testis
It is usually possible to ‘get above the lump’ on examination
Adhesive capsulitis associations
diabetes
Adhesive capsulitis features
Features typically develop over days
external rotation is affected more than internal rotation or abduction
both active and passive movement are affected
patients typically have a painful freezing phase, an adhesive phase and a recovery phase
bilateral in up to 20% of patients
the episode typically lasts between 6 months and 2 years
