Things I got Wrong Pt. 3 Flashcards

(180 cards)

1
Q

Where are venous ulcers found?

A

In the gaiter area, typically above the medial malleolus

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2
Q

What antibiotics are recommended for an infective exacerbation of COPD?

A

Amoxicillin, doxycycline, or clarithromycin.

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3
Q

How is HFpEF managed?

A
  • Lifestyle advice
  • ACEi if the patient is hypertensive
  • Furosemide if they are overloaded
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4
Q

What is an indication for LTOT in COPD?

A

A PaO2 score of between 7.3 and 8 with the presence of peripheral oedema is one of the indications for long-term oxygen therapy
OR, a <7.3 kPa alone

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5
Q

What causes AF?

A

A. SMITH
-Alcohol binge
Sepsis
- Mitral Valve Pathology (stenosis - increases in left atrial pressure)
- Ischemic Heart Disease
- Thyrotoxicosis
- Hypertension

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6
Q

How long should patients be anticoagulated before cardioversion?

A

3-4 weeks of apixaban

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7
Q

What is congestive heart failure?

A

Congestive heart failure which is a combination of right and left sided heart failure

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8
Q

What are the signs and symptoms of right sided HF?

A

Right sided heart failure often presents with peripheral oedema (pedal, scrotal or sacral), raised JVP, hepatomegaly and bloating

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9
Q

What are the signs and symptoms of left sided heart failure?

A

Orthopnoea, paroxysmal nocturnal dyspnoea, exertional dyspnoea, pink frothy sputum (because of blood and fluid being backed up into the lungs coming up in a cough), pulmonary oedema

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10
Q

What are the ABPI cut offs for mild, moderate and severe PAD?

A

Normal - 1-1.4
Mild - 0.8-0.9
Moderate - 0.5-0.8
Severe <0.5

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11
Q

What investigations can be carried out for PAD?

A

ABPI
Duplex arterial ultrasound: beneficial for individuals who might be suitable for revascularisation.
MR arteriogram: utilised for those who are candidates for revascularisation.

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12
Q

What is used for the definitive diagnosis of biliary atresia?

A

Cholangiography

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13
Q

When are NSAIDs contraindicated for gout?

A

CKD3< and peptic ulcers

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14
Q

What investigations might be ordered for someone presenting with ?PMR?

A

Urine dipstick may be positive for blood due to myoglobin released in myositis
ESR and/or CRP are usually moderately raised in PMR
FBC - raised white cells may indicate infection, anaemia may be seen in malignancy or due to chronic disease
U&Es may show renal impairment in myeloma or infection
LFTs may be deranged e.g. due to metastatic cancer or a high ALP in osteomalacia
Bone profile may show high calcium in myeloma, or low calcium in osteomalacia
Creatine kinase will be raised in myositis
Thyroid function tests for hypo or hyperthyroidism
Protein electrophoresis to screen for myeloma; urine Bence Jones protein should be considered
Rheumatoid factor as a screen for rheumatoid arthritis, ANA and anti-CCP antibodies should also be sent if there is clinical suspicion
HbA1c prior to starting steroids due to their impact on blood glucose control

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15
Q

How is prostate cancer investigated?

A

DRE - irregular, hard prostate with loss of central sulcus (2ww)
PSA
Multiparametric MRI - assessed on a scale of 1-5
Prostate biopsy is performed if the MRI shows 3<

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16
Q

What is a common, non neurological side effect of levadopa?

A

Constipation

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17
Q

Which medications can exacerbate psoriasis?

A

Beta-blockers, antimalarials and lithium

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18
Q

Why are chemo patients prescribed prophylactic allopurinol?

A

Chemotherapy leads to cell death and a surge of uric acid - leading to an acute flare of gout

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19
Q

What kind of drug is tamsulosin?

A

Alpha 1 antagonist

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20
Q

What is a side effect of tamsulosin and which is it contraindicated in?

A

Orthostatic hypotension, contraindicated in a history of falls

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21
Q

What kind of drug is finasteride?

A

5 alpha reductase inhibitor

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22
Q

What are the 2 main pathophysiological mechanisms of COPD?

A

Bronchitis and emphysema

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23
Q

What is the pathophysiology of bronchitis?

A

As a protective reaction to smoke or other pollutants, goblet cells hypersecrete mucus in the bronchi and bronchioles of the lungs. Cilia are not able to remove the excess mucus and so it obstructs the small airways. Ongoing inflammation causes remodelling and thickening of the airway walls that also contributes to obstruction.

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24
Q

What is the pathophysiology of emphysema?

A
  • Inflammation in the lungs is usually countered by antiproteases such as alpha-1 antitrypsin, however the activity of these is reduced by smoke and other pollutants.
  • Without sufficient antiprotease activity, proteolytic enzymes produced by inflammatory cells break down the walls of the alveoli.
  • This causes enlargement of the terminal airspaces and reduces the surface area available for gas exchange.
  • Impaired gas exchange and gas becomes trapped ⇒ BULLAE (large air sacs)
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25
What are the criteria for a clinical diagnosis of osteoarthritis?
The patient is aged over 45 years AND The patient has activity-related joint pain AND The patient has no morning stiffness or the morning stiffness lasts less than 30 minutes
26
What is the best way to manage opioid related constipation?
Opioid-related constipation is best treated with a combination of osmotic and stimulant laxatives
27
What are the functions of the kidney?
- Excretion of byproducts of metabolism (urea, creatinine, drugs) - Excretion of phosphate, absorption of Ca2+, activation of vitamin D - Fluid balance and BP (RAAS) - Electrolyte balance and pH (if pH drops, the intercalated cells of the collecting duct start to reabsorb more bicarb and excrete more H+) - RBC production via EPO - Prevention of protein loss through the basement membrane
28
Function of aldosterone:
Aldosterone regulates the salt and water balance of the body by increasing the retention of sodium and water and the excretion of potassium by the kidneys
29
What are the causes of CKD?
- **Diabetes mellitus** - HTN/atherosclerotic renal vasculature => hypertensive nephrosclerosis - Glomerulonephritis - Infective (chronic pyelonephritis) - Obstructive (including kidney stones, vesicoureteric reflux) - Cystic or congenital (autosomal dominant polycystic kidney disease, IgA nephropathy) - Progressing AKI - more common in elderly people with lots of comorbidities
30
Using the CKD staging chart, at which point is CKD diagnosed?
CKD is diagnosed above G2 and A1
31
What are the criteria for A1-3 in terms of CKD staging?
A1 = <30 A2 = 30-300 A3 = >300
32
What are some RFs for CKD?
Diabetes, hypertension, PCKD, lupus, male, smoking, exposure to nephrotoxic drugs (gentamicin for example)
33
How is CKD diagnosed?
- Bloods: eGFR of <60ml/min/1.73 m 2 measured on at least 2 occasions 90 days apart, with markers of kidney damage such as proteinuria, constant haematuria of renal origin, electrolyte or histological abnormalities, might show anaemia of chronic disease - Urine: albumin creatinine ratio >3 - Renal US - done if complications are suspected
34
How is CKD managed?
- Statins to reduce lipids - ACEi to control BP and proteinuria - Avoid nephrotic drugs - EPO infusion if anaemic - Dietician to reduce phosphate in diet, or phosphate binders - Vitamin D and calcium supplements - In CKD 5, haemodialysis or peritoneal dialysis, or even a kidney transplant
35
What is the management of erectile dysfunction?
1. Psychosexual counselling 2. Viagra 3. Vacuum assisted device
36
Why is vitamin D low in CKD?
Reduced alpha hydroxylase 1 expression (the kidney is involved in activating it)
37
How is CVD risk managed in CKD?
Statins, stop smoking, healthy eating, exercise
38
How is BP and proteinuria managed in CKD?
ACEi => normal BP management guidelines
39
How is anaemia managed in CKD?
- Iron replacement if deficient - EPO if not (anaemia of chronic disease)
40
How is acidosis managed in CKD?
- Regular monitoring - Sodium bicarbonate tablets if they become acidotic (intercalated cells in the collecting duct secrete H+ and absorb HCO3- but they begin to lose this ability)
41
How is mineral bone disease managed in CKD?
- Vitamin D can be given to help in MBD - alfacalcidiol or calcitriol - Referral to dietician so pts can learn how to reduce intake of phosphate - dairy, processes meats, ready meals - if this doesn’t work they can take phophate binders - clacium carbonate and calcium acetate bind phosphate in the gut so it cannot be absorbed - Bisphosphonates can be used to treat osteoporosis
42
What types of kidney replacement therapy are available in CKD?
- haemodialysis - peritoneal dialysis - transplant
43
What are some risk factors for candidiasis?-
Pregnancy Antibiotic use Poorly controlled diabetes SGLT2 inhibitors Immunosuppression
44
How can candidiasis be diagnosed?
- Charcoal swab - pH to differentiate BV
45
What is the pathophysiology of BPH?
- BPH arises as a result of the loss of homeostasis between cellular proliferation and cell death - This results in hyperproliferation of epithelial and stromal cells in the transition zone of the prostate - Enlarged prostate compresses the urethra, leading to issues with urine flow and hesitancy and difficulty initiating flow - Enlarged prostate also puts pressure on the bladder, leading to frequent urination
46
What are some signs of BPH?
- Hesitancy – difficult starting and maintaining the flow of urine - Weak flow - Urgency – a sudden pressing urge to pass urine - Frequency – needing to pass urine often, usually with small amounts - Intermittency – flow that starts, stops and varies in rate - Straining to pass urine - Terminal dribbling – dribbling after finishing urination - Incomplete emptying – not being able to fully empty the bladder, with chronic retention - Nocturia – having to wake to pass urine multiple times at night
47
How is BHP investigated?
Bladder diary International Prostate Symptom Score DRE PSA
48
How is BPH managed?
Alpha blockers - relax the urethral sphincter (postural hypotension) 5 alpha reductase inhibitors - reduce the size of the prostate as this enzyme converts testosterone to dihydrotestosterone (more potent androgen) Transurethral resection / vaporisation of the prostate - removing part of the prostate from inside the urethra using a resectoscope and a diathermy loop to shave away prostatic tissue
49
What antihistamine is used in obstetric cholestasis?
Chlorphenamine
50
What abnormality is seen in pyloric stenosis?
Hypochloraemic hypokalaemic metabolic alkalosis
51
What should you do if a child with bronchiolitis is having apnoeic episodes?
Immediate admission to hospital
52
What are the red flag criteria for bronchiolitis?
Apnoea (observed/ reported) Child looking unwell to a healthcare professional Severe respiratory distress/ grunting/ marked chest recession Clinical dehydration, 50-75% of their normal milk intake RR >70 Central cyanosis O2 Sat <92%
53
What is the acute management of congenital adrenal hyperplasia?
IV fluids, dextrose, hydrocortisone
54
What could cause an absent fundal reflex on neonatal examination with an ophthalmoscope?
Retinoblastoma, congenital cataracts
55
What are some symptoms of tetralogy of fallot?
Recurrent chest infections Poor feeding Breathlessness Cyanosis whilst feeding/crying Harsh ejection systolic murmur
56
Who should notifiable diseases be reported to?
UKHSA (UK Health Services Agency) local health protection team within 24 hours, immediately (don't need to wait for confirmaiton)
57
How are juvenile myoclonic seizures managed?
Boys - sodium valproate Girls - leviteracitam
58
Is carbamazepine recommended in myoclonic seizures? Why?
No - it can worsen myoclonus
59
What is the pathophysiology of Duchenne's muscular dystrophy?
Gene mutation on Xp21 Dystrophin is absent, which is important for muscle architecture Muscle is lost and replaced by adipose tissue
60
How is DMD diagnosed?
serum creatine kinase (CK), electromyogram (EMG), muscle biopsy, genetic testing, muscle MRI (3 marks max)
61
How is DMD managed?
Medical - corticosteroids, vitamin D and calcium supplements, creatine supplements Surgical - correct contractures, scoliosis surgery Monitoring for complications - respiratory and cardiac Physiotherapy - provide exercises OT - provide equipment Education Counselling Palliative care
62
What are some complications of DMD?
Global developmental delay Loss of ambulation, contractures Dilated cardiomyopathy and heart failure Learning disability Respiratory failure Obstructive sleep apnoea Scoliosis
63
How long does physiological jaundice last in term babies and preterm babies?
Term - 2 weeks Pre-term - 3 weeks
64
What are the treatments for neonatal jaundice?
Phototherapy Exchange transfusion
65
What are the risk factors for glue ear?
Age: Children between the ages of 6 months and 2 years are more susceptible to ear infections due to the anatomy of their developing Eustachian tubes. 2. Bottle Feeding while Lying Down: Feeding infants while lying down can increase the risk of milk or formula entering the Eustachian tubes, promoting bacterial growth. 3. Allergies: Children with allergies, especially to environmental factors like pollen or pet dander, may have an increased risk of ear infections. 4. Genetic Predisposition: A family history of recurrent ear infections may increase a child's susceptibility to similar issues. 5. Cleft Palate: Structural abnormalities, such as cleft palate, can affect the function of the Eustachian tube and increase the likelihood of infections. 6. Respiratory Infections: Children who experience frequent respiratory infections, such as colds or sinus infections, are more prone to developing ear infections.
66
What is the importance of middle ear ventilation in glue ear? What happens if this is not done?
Middle ear ventilation is crucial for equalising pressure, preventing fluid buildup, and maintaining optimal hearing. If this is not done, the child may suffer with hearing difficulties
67
How can glue ear be managed?
Conservative: nasal saline irrigation, usually resolves in 3m Medical: antibiotics in cases of acute exacerbations. Surgical: tympanostomy tube insertion may be considered in persistent cases (>3m, repeated episodes, 25-30 decibels hearing loss, speech and language delays, struggling at school)
68
What is the pathophysiology of glue ear?
- The Eustachian tube connects the middle ear to the back of the throat - this helps drain secretions from the middle ear. - It usually keeps the air pressure on both sides of the eardrum equal. - In young children as the tube is narrower, so it is easier to block - This can happen after a cold for example - If the tube is blocked, this makes the air pressure inside the middle ear drop. Fluid drains from the surrounding tissue to fill up the middle ear. With time, this fluid becomes sticky and stops the eardrum and ossicles vibrating as they should - This causes hearing loss
69
What investigations might be performed in glue ear?
- Otoscopy - shows a dull tympanic membrane with air bubbles or a visible fluid level, no light reflex - Pneumatic otoscopy - decreased movement of the tympanic membrane on air insufflation due to effusion in the middle ear - Tympanometry (I think this is what the lady did to me in Chesterfield) - tests the mobility of the eardrum and may show a poor compliant eardrum with reduced movement - Audiology - may show hearing loss
70
What is the pathophysiology of VUR?
Abnormal backflow of urine from the bladder into the ureter/kidney, due to lateral displacement of the ureters (inadequate function of the vesico-ureteric junction)
71
What are the grades of VUR?
1 - reflux into the ureters 2 - reflux into the renal pelvis on micturition 3 - mild dilation of the ureter, renal pelvis and calyces 4 - moderate dilation of the ureter, renal pelvis and calyces with moderate ureteral torturosity 5 - severe dilation of the ureter, pelvis and calyces with torturosity
72
What investigations should be done for VUR?
- micturating cystourethrogram to identify reflux under x-ray - DMSA scan to look for renal scarring
73
How is VUR managed?
Conservative: - Long-term, low-dose antibiotic prophylaxis to prevent urinary tract infections (UTIs), which can lead to renal scarring - Regular monitoring with renal ultrasound and micturating cystourethrogram (MCUG) - Patient education, including scheduled voiding times, avoiding constipation an ensuring adequate fluid intake in children Surgery: - Open or laparoscopic ureteric reimplantation (not routinely done)
74
What are some risk factors for UTIs in children?
age <1 year, female sex, white children, uncircumcised boys <1 year, previous UTI, sexual abuse, bladder/bowel dysfunction, not breastfed, previous surgery to uterine tract, anatomical abnormalities (e.g. VUR, obstruction, posterior urethral valves, ureterocele, nephrolithiasis), immunosuppression, malnourishment, dysfunctional elimination syndrome (‘holding on’ to urine), poor hygiene (e.g. frequent soiling, wiping back to front in girls)
75
Are MSUs required to investigate UTIs in children?
MCS is diagnostically as useful as urinalysis (according to NICE). It is only recommended if the child: - Is thought to have pyelonephritis - A high/intermediate risk of serious illness - Under 3m - Has recurrent UTIs - Isn't repsonding to treatment within 24-48 hours - Has clinical symptoms but the urinalysis is negative
76
What are the criteria for an US in children with UTIs?
- All children ***under 6 months*** with their first UTI should have an abdominal ultrasound within 6 weeks - Children with ***recurrent UTIs*** should have an abdominal ultrasound within 6 weeks - Children with ***atypical UTIs*** should have an abdominal ultrasound during the illness
77
What mode of imaging is used to diagnose NEC, and what would it show?
- Dilated loops of bowel - Intramural gas (pneumatosis intestinalis) - Bowel wall oedema - if there has been a perf: pneumoperitoneum, Rigler's sign, Football sign
78
What are the risk factors for NEC?
* Very low birth weight (1 mark) ● Prematurity (1 mark) ● Formula feeds (it is less common in babies fed by breast milk feeds) (1 mark) ● Respiratory distress (1 mark) ● Assisted ventilation (1 mark) ● Sepsis (1 mark) ● Patent ductus arteriosus (1 mark) ● Congenital heart disease (1 mark)
79
How is NEC managed?
- NMB - IV fluids - TPN - Antibiotics IV - NG tube to drain fluid and gas from the abdomen - Surgery to remove the dead portion of bowel
80
Why does NEC develop?
- The inability of the immature gut to secrete its normal biochemical defenses - inadequate blood circulation to the gut - inability of the infant's digestive syste, to keep out dangerous bacteria - Inadequate ability of the immature intestine to provide an adequate structural barrier to bacteria. - inability to digest the food passing through it, leading to the buildup of toxic food substances
81
What are some complications of NEC?
● Perforation and peritonitis (1 mark) ● Sepsis (1 mark) ● Death (1 mark) ● Strictures (1 mark) ● Abscess formation (1 mark) ● Long term stoma (1 mark) ● Short bowel syndrome after surgery
82
What is haemolytic uraemic syndrome?
Haemolytic uraemic syndrome (HUS) involves thrombosis in small blood vessels throughout the body
83
What causes HUS?
Gastroenteritis - E. coli O157 (EHEC) or Shigella
84
What is the triad of HUS?
- Microangiopathic haemolytic anaemia (haemolysis due to pathology in the small vessels (microangiopathy). Thrombi partially obstruct the small blood vessels and churn the red blood cells as they pass through, causing them to rupture) - Acute kidney injury - Thrombocytopenia (the formation of blood clots consumes platelets)
85
What are the signs of HUS?
Initially signs of gastroenteritis, which turns bloody after several days. Fever Abdominal pain Lethargy Pallor Reduced urine output (oliguria) Haematuria Hypertension Bruising Jaundice (due to haemolysis) Confusion
86
How is HUS managed?
Medical emergency!!! Admission to hospital!! Supportive management of: Hypovolaemia (e.g., IV fluids) Hypertension Severe anaemia (e.g., blood transfusions) Severe renal failure (e.g., haemodialysis)
87
What is seen on a blood film of HUS?
Schistocytes or helmet cells
88
What is required for definitive diagnosis of ALL?
Bone marrow biopsy
89
What abnormalities might be seen in tumour lysis syndrome?
Raised uric acid, raised K+, raised phosphate, low calcium (due to raised phosphate)
90
What are some poor prognostic factors for ALL?
● age <2 years or >10 years ● WBC >20 * 109/l at diagnosis ● T or B cell surface markers ● non-Caucasian ● male sex
91
What is the differnce between IgE and non-IgE mediated CMPA?
● IgE-mediated CMPA has rapid reaction occurring within 2 hours of ingestion. Non-IgE-mediated CMPA has a delayed reaction, occurring >2 hours to days. ● IgE-mediated reactions can include anaphylaxis, while non-IgE reactions are more commonly gastrointestinal.
92
What complications of coeliac disease might occur?
● Vitamin deficiency ● Anaemia ● Osteoporosis ● Ulcerative jejunitis ● Enteropathy-associated T-cell lymphoma (EATL) of the intestine ● Non-Hodgkin lymphoma (NHL) ● Small bowel adenocarcinoma (rare)
93
What should you do if a child comes in with symptoms of transient synovitis / septic arthritis?
Urgent referral to paediatrics for a speicalist review
94
What is a toddler's fracture?
Spiral fracture of the tibia
95
How is CAH managed?
- Hydrocortisone and fludrocortisone replacement - Females might need corrective surgery on their genitals - GH therapy might be used asthey tend to have a short stature (somatropin)
96
What is the pathophysiology of HUS?
Blood clots form in small blood vessels predominantly in the kidney, triggered by the shiga toxin. This causes thrombolysis, haemolytic anaemia and AKI
97
In patients with asthma uncontrolled by a MART inhaler, what comes next?
In adults with uncontrolled asthma on MART, FeNO and blood eosinophil levels should be re-checked to guide further managemen
98
What is a MART inhaler?
Steroids and a LABA
99
When should bisphosphonates be started?
They should be started in women with either confirmed osteoporosis by DEXA scanning or >75 years with two or more risk factors for fracture or a previous fragility fracture
100
What is first line for haemarrhoids?
Increase dietary fibre and fluid intake
101
What are megaloblastic features of anaemia on a blood film?
Large immature red blood cells and hypersegmented neutrophils.
102
What are some signs of OA on an x-ray?
LOSS Loss of joint space Osteophytes Subchondral sclerosis Subchondral cysts Squaring of th ethumb
103
What are the doses of adrenaline for different age groups?
- Children <6 months of age: 100-150 micrograms (0.1 to 0.15 mL) - Children 6 months to 6 years of age: 150 micrograms (0.15 mL) - Children 6-12 years of age: 300 micrograms (0.3 mL) - Children >12 years of age and adults: 500 micrograms (0.5 mL)
104
What are the different degrees of severity for eczema?
- Mild - areas of dry skin, and infrequent itching (with or without small areas of redness) - Moderate - areas of dry skin, frequent itching, and erythema (with or without excoriation and localized skin thickening) - Severe - widespread areas of dry skin, incessant itching, and erythema (with/without excoriation, extensive skin thickening, bleeding, oozing, cracking, and alteration of pigmentation) - Infected - if eczema is weeping, crusted, or there are pustules, with fever or malaise
105
What is the treatment for mild eczema?
Mild eczema - liberal emollient usage + mild topical corticosteroid (such as hydrocortisone 1%) for areas of red skin.
106
What is the treatment for moderate eczema?
Moderate eczema - liberal emollient usage + moderate topical corticosteroid (such as clobetasone butyrate 0.5% - Eumovate) for 5 days. Hydrocortisone 1% should be used for the face and flexures. Consider prescribing maintenance topical corticosteroids to control areas of skin prone to frequent flares.
107
What is the treatment for severe eczema?
Severe eczema - liberal emollient usage + potent topical corticosteroid (for example betamethasone valerate 0.1% - Betnovate) to be used on inflamed areas. For the face and flexures, use a moderate potency corticosteroid (such as Eumovate).
108
Name some types of birth mark:
* Haemangioma * Erythema toxicum neonatorium * Milk spots (milia) * Mongolian blue spot (congenital dermal melanocytosis) * Port wine stain (naevus flammeus) * Naevus * Cafe au lait spot
109
How can allergic rhinitis be managed?
* Hayfever lol * Avoid the trigger * Take some antihistamines * Nasal corticosteroid sprays (fluticasone, mometasone)
110
Which medications can cause Steven's Johnson Syndrome / TEN?
- Anti-epileptics (lamotrigine) - Antibiotics like penicillins and cephalosporins - Allopurinol - NSAID
111
What is the pathophysiology of Steven's Johnson Syndrome / TEN?
A disproportional hypersensitivity response causes epidermal necrosis, resulting in blistering and shedding of the top layer of skin
112
What is the progression of SJS and TEN?
* Starts with fever, cough, sore throat, itchy skin etc after taking the med * Develops into a red erythematous macular rash (dark in the middle, light on outside) * After a few days, these begin to blister and the skin sloughs away, leaving raw skin underneath (Nikolsy sign) * Mucosal ulceration is also present (conjunctiva, mouth, pharynx, GIT)
113
How is SJS/TEN managed?
* Stop the offending drug * Analgesia * Antiseptics * Wound care * Skin care * Fluid and electrolyte management * Referral to ophthalmology
114
How is SJS / TEN diagnosed?
* Normally clinical * Skin biopsy might show keratinocyte apoptosis and detachment of the epidermal layer from the dermal layer
115
What HbA1c indicates diabetes, prediabetes and normal?
* Diabetes = 48 (6.5%) * Pre-diabetes = 42-47 * Normal = <42% (<5.6%)
116
On an OGTT, what are the criteria for pre diabetes?
- Impaired fasting glucose >6 but <7 - Impaired glucose tolerance <11.1 but >7.8
117
How often is HbA1c tested?
Every 3-6 months until stable
118
In adults, a clinical history alone may be enough to diagnose T1DM. What are the criteria?
If they have hyperglycaemia, ketosis, rapid weight loss, ages <50, low BMI, family history of autoimmune disorders etc
119
What testing might be done to diagnose T1DM if there is diagnostic uncertainty?
* C peptide * Auto-antibodies (anti-insulin, anti islet cell, anti GAD)
120
What testing might be done to diagnose T1DM?
* Fasting BM * Random BM * OGTT
121
How does impaired insulin action/production lead to high blood sugars?
* Less insulin to move glucose into cells * Glucagon thinks you have low sugar, so it continues to break down glycogen (glycogenolysis) * Liver thinks you have low sugar, so it carries out lipolysis and proteolysis (gluconeogenesis)
122
What education programs are available for T1 and T2 diabetes?
* DAFNE - T1DM, dose adjustment for normal eating * DESMOND - diabetes education and self management for ongoing and newly diagnosed
123
Which diabetic medications carry a risk of hypoglycaemia?
* Insulin * Sulphonylureas
124
How do metformin and pioglitazone work?
Increases insulin sensitivity and decreases liver production of glucose
125
What are some examples of DPP-4 inhibitors?
Sitagliptin
126
What is the mechanism of DPP-4 inhibitors?
- In normal physiology, GLP-1 is degraded by DPP-IV so appetite can return - If the breakdown of GLP-1 is inhibited, these effects will persist for longer - Inhibition achieved through competitive inhibition - Increase in satiety, reduction in appetite, modest increase in insulin levels and modest glucagon lowering effect, but no improvement in CVD risk
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For which patients are GLP analogues introduced as a fourth line therapy?
* BMI >35 and triple therapy has failed
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Which diabetic drugs can cause weight gain?
* Sulphonylureas * Pioglitazone
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What fluids are given for DKA?
* Bolus - 10 ml/kg 0.9% sodium chloride * Maintenance - for kids, the usual calculations, for adults give 500 * K+ is added to the fluids
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What insulin is given in DKA?
Fixed rate insulin infusion 0.1 unit/kg/hour - actrapid, 1-2 hours after fluids
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What should you do in DKA, when the patient's BM reaches <14?
- Once blood glucose is < 14 mmol/l an infusion of 10% dextrose should be started at 125 mls/hr *in addition* to the 0.9% sodium chloride regime - Switch to oral once they are altert and can take oral fluids without nausea and vomiting
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What are the criteria for DKA?
- Hyperglycaemia (plasma glucose >11) - Raised plasma ketones (urine ketones > 2+) - Metabolic acidosis – <7.3 pH and HCO3 <15
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What are the criteria for DKA resolution?
- pH >7.3 and - blood ketones < 0.6 mmol/L and - bicarbonate > 15.0mmol/L
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How is a hypo managed in an alert patient?
- Short acting carbs - glucose gel, sweets Followed by: - Long acting carbs - bread, pasta
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How is a hypo managed in an unconscious patient in the community?
IM glucagon
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How is a hypo managed in an unconscious patient in hospital?
IV 2ml/kg 10% dextrose
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What antibodies are found in Hashimoto's disease?
Anti-thyroglobulin, anti-thyroid peroxidase
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Why does hypothyroidism cause a goitre?
The thyroid gland is constantly stimulated by TSH
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Is levothyroxine T3 or T4?
Synthetic T4
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What antibodies are present in Grave's disease?
* Thyroid receptor antibodies - IgG
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Other than bloods, what investigations are available for thyroid disease?
* Isotope uptake scan - Grave's would show an increased blood flow and would appear bright
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What regimes are available for hyperthyroidism treatment?
* Block and replace * Block-titrate
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What is first line for hyperthyroidism?
* Carbimazole and propanolol * Propylthiouracil is better for young women as carbimazole is teratogenic
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What are the potential treatments for hyperthyroidism?
* Antithyroid drugs (carbimazole, propylthiouracil) * Radioiodine 131 I * Symptomatic management (beta blockers) * Surgery (thyroidectomy)
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What are the first, second and third line treatments for varicose veins?
Conservative - lose weight, elevate the legs, compression stockings 1 - endothermal ablation 2 - sclerotherapy 3 - surgical stripping
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What antibodies are found in Grave's disease?
Thyroid receptor antibodies, such as thyroid-stimulating immunoglobulins (TSIAb) or thyrotropin receptor antibodies (TRAb)
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What is the mechanism of action of carbimazole?
Prevents the thyroid peroxidase enzyme (TPO) from coupling and iodinating the tyrosine residues on thyroglobulin. Thyroglobulin, following the coupling and iodinating process, would normally then be degraded to produce thyroxine (T4) and tri-iodothyronine (T3). Hence, by blocking TPO, Carbimazole reduces the production of the thyroid hormones T3 and T4
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What should patients with diabetes and hypertension be started on?
White patients should be started on ACEi. Patients of Afro-Caribbean origin with type 2 diabetes who are diagnosed with hypertension should be treated with an ARB first line.
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What are some red flags that hypertension needs further investigation?
Malignant HTN Resistant HTN ROPE - renal disease, obesity, pregnancy, endocrine disorders
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What additional investigations should be done in someone newly diagnosed with hypertension?
- Urine albumin:creatinine ratio for proteinuria and dipstick for microscopic haematuria to assess for kidney damage - Bloods for HbA1c, renal function and lipids - U&Es, serum total cholesterol, HDL - Fundus examination for hypertensive retinopathy - ophthalmoscopy - ECG for cardiac abnormalities - QRisk3
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What are the thresholds for treatment in hypertension?
- Peeps at low CVD risk: start treatment if above 160/100 in surgery - Peeps at high CVD risk: start treatment if above 140/90 in surgery - >180/120 - refer for specialist assessment if signs of retinal haemorrhage, papillodema, life threatening symptoms (confusion, CP, HF, AKI)
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What is the mechanism of thiazide like diuretics?
Inhibition of Na+/Cl- transporter
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What is paroxysmal AF?
AF suddenly comes and goes, for normally less than a week at a time, probably because the tissue is still relatively healthy and normal contraction is still possible
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What is persistent AF?
The AF episodes no longer terminate spotaneously, and last over a week straight
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What is long standing persistent AF?
lasts for longer than 12 months without terminating
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What is permanent AF?
Doctor and patient make a conscious decision to stop trying to correct the rhythm
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In angina, what can be used if BB and CCB are contraindicated/nottolerated/ineffective?
* ivabradine, nicorandil, ranolazine
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What is a normal ejection fraction?
55-70%
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What is HF with reduced ejection fraction vs preserved ejection fraction?
Reduced - <50 Preserved - >50
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What is the pathophysiology of HF with reduced ejection fraction?
- Systolic failure - Impaired pumping - Left ventricle doesn't contract very well, reducing the stroke volume and cardiac output. This means the LV becomes overloaded and begins to back up into the lungs, leading to pulmonary hypertension and oedema
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What is the pathophysiology of HF with preserved ejection fraction?
- Diastolic failure - Impaired filling / ventricular relaxation - Ventricles are poorly compliant, which means they can't relax or fill very well during diastole. This means the stroke volume is reduced, but EF is proportionally preserved
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What are the causes of left sided heart failure with preserved ejection fraction?
* Restrictive - amyloidosis, sarcoidosis * Valve disease - increased afterload, heart becomes hypertrophied and stiff, doesn't relax as well * Hypertension - increased afterload, heart becomes hypertrophied and stiff, doesn't relax as well
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What are the causes of left sided heart failure with reduced ejection fraction?
* Hypertension * Coronary artery disease * Arrhythmia * Mitral or aortic regurge
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What is the pathway of investigation for HF?
- If previous MI, go straight to TTE. - If no previous MI, do BNP - If BNP > Above 4000pg/ml -> urgent TTE - If BNP > 100 - 4000pg/ml -> TTE within 6 weeks
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When might ivabradine be indicated in HF?
As a fourth line treatment in people who's EF <35% and HR sinus and >75
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When are hydralazine and nitrates indicated in HF?
Fourth line in black people - if added to ACEi, BB and aldosterone antagonists in black people it restores the efficacy of ACEi
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When is digoxin indicated in HF?
Can be useful for symptom control of arrhythmias in sedentary people
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What are the risk factors for rheumatoid arthritis?
* Smoking * Family history * Female * Middle aged - 50+
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What are the symptoms of rheumatoid arthritis?
Symmetrical distal polyarthropathy - commonly in the PIP, MCP, wrist, ankle, metatarsophalangeal joints, cervical spine - NOT DIP! Pain worse in the morning >30m after long periods of inactivity that improves with movement, boggy swelling
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What are the extra-articular manifestations of rheumatoid arthritis?
* SPENG * Sjogren's * Pericarditis * Effusions * Nodules * Glomerulonephritis Associated with a worse prognosis!
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What are the signs of rheumatoid arthritis?
- Boggy feeling in the synovium around the joints upon palpation - Z shaped deformity of the thumb - Swan neck deformity (hyperextended PIP with flexed DIP) - Boutonnieres deformity (hyperextended DIP with flexed PIP) - Ulnar deviation
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What investigations might be performed for rheumatoid arthritis?
* Bloods - anti-CCP, rheumatoid factor, raised CRP and ESR * X-rays - LOSE - loss of joint space, osteopenia, soft tissue swelling, erosions (subchondral) * US - synovitis, soft tissue swelling
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What classification criteria can be used to diagnose rheumatoid arthritis?
American College of Rheumatology/European League Against Rheumatism (ACR/EULAR)
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What scoring systems can be used to asses RA?
The Health Assessment Questionnaire (HAQ) measures self-reported functional ability. The Disease Activity Score 28 Joints (DAS28) score is used in monitoring disease activity and response to treatment. It involves assessing 28 joints and assigning points for: Swollen joints Tender joints The ESR or CRP result Repeated monthly until disease is under control
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How are flares of rheumatoid arthritis managed?
* Ice/splinting * Short course of PO steroids * Intraarticular steroids if it's localised pain * NSAIDs can improve pain * These aim to induce remission
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How is chronic rheumatoid arthritis managed?
1. Hydroxychloroquine is first line in mild disease 1. Methotrexate, sulfasalazine, leflunomide in moderate to severe disease 2. 2 of these in combo 3. Methotrexate + anti-TNF (adalimumab, infliximab) 4. Methotrexate + anti-CD20 (rituximab)
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What screening does someone need before being started on TNF alpha inhibitors?
Chest X-ray for latent TB - it can reactivate it
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What RA treatments are safe in pregnancy?
Hydroxychloroquine, sulphasalazine
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What are the components of a FRAX score?
Age, height, weight, steroid use, RA, previous fracture, parental hip fracture, smoking, drinking >3 units a week
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What is the progression of treatment in endometriosis?
Ibuprofen and paracetamol Hormonal treatments like COCP and the coil GnRH needs to be initiated by a specialist