In The Wards

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[biomedicalephemera]

Dermatomes of the Adult Male

A dermatome is an area of the body supplied by a single spinal nerve ganglion. Physical sensations (and as such, autonomic/spinal reactions) are controlled by these nerves.

Technically “dermatome” only refers to the skin supplied by that nerve (derma - “skin”, -tome “single section”), but as the lower graphics show, we’ve also determined what nerves control the sensations of our muscles.

As you can see in the graphic of the trigeminal nerve innervation at the top, there’s a moderate amount of variation between individuals, but the basic layout is generally the same.

Because the basic layout of our nerves is known, when someone damages a nerve, which nerve has been damaged can sometimes be determined by what area of the skin has abnormal sensations. A few years ago, I damaged my elbow at work, and it was determined that my ulnar nerve had been affected, due to the lower third of my arm and hand being numb. Thankfully it’s since recovered, but in some situations, nerve damage can cause permanent altering of sensation in the parts of the body affected.

Atlas of Applied (Topographical) Human Anatomy for Students and Practitioners. J. Howell Evans, 1906.

[mynotes4usmle]

Abdominal Aorta’s Branches

[mynotes4usmle]

Zoomed in for @drmuqs :)  Sorry for the late response!

[medicowesome]

Conn’s syndrome mnemonic

Hi. I keep forgetting that Conn’s syndrome is hyperaldosteronism. Can you help me out with this?

Sure! :D

The N’s are for sodium - Hypernatremia!

The C makes a K for potassium, which is less than the number of N’s, therefore, hypokalemia!

Also, Na+ is sodium. A could remind you of Aldosterone. AL could remind you of ALkalosis.

That’s all!

-IkaN

[jewsee-medicalstudent]

Common painkillers.

No, this isn’t the Judas Priest song (furthermore I like it). This is a guide to drugs used to stop pain, maybe the most used drugs with cardiovascular drugs and antidepressant. Painkillers, or analgesics, come in a number of forms, but fall broadly into two main classes: non-steroid anti-inflammatory drugs (NSAIDs) and opioids. This graphic takes a look at a selection of common painkillers, their common brand names, and how they work.

Non-steroid anti-inflammatory drugs include analgesics such as aspirin and ibuprofen, shown in the graphic, as well as naproxen. These drugs all work by inhibiting the synthesis of a class of chemical compounds called prostaglandins. Prostaglandins are produced by the body during inflammation, and they contribute significantly towards pain. NSAIDs work by inhibiting the activity of two enzymes, cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2). These enzymes catalyse prostaglandin synthesis, so when their activity is inhibited, so is the body’s manufacture of prostaglandins. The net result is a reduction in inflammation, and subsequently a reduction in pain. Painkillers have no innate method of reaching only the site of pain, but rather are distributed evenly through-out the body when you take them. They’re also non-discriminative in terms of their action, and will inhibit prostaglandin synthesis all over your body, not just at the site of pain. Prostaglandins don’t just have a role in pain in our bodies – they’re also found in the gut, where their role includes protection of the gut lining. As such, use of NSAIDs increases the risk of stomach ulcers and gastrointestinal irritation. For this reason, during sustained course of NSAIDs (for example, after surgery), drugs to help protect the gut lining may also be prescribed.

Opioids are the second major class of painkillers. These are a class of drugs related to morphine, the compound found in significant concentrations in the opium poppy. The opium poppy itself has been used for its natural painkilling properties for centuries, as the opium which can be extracted from it contains around 12% morphine. The synthetic drug heroin is also obtained from a simple chemical modification of morphines structure; many of the painkilling opioids have similarly minor differences in chemical structure. The opioids work in a different way to the NSAIDs; rather than combatting the pain at its source, they instead prevent the sensation of pain by binding to and blocking the receptors in the brain and spinal cord that are responsible for the transmission of the sensation of pain. This group of receptors are known as opioid receptors, and there are four different subtypes; the exact manner in which many of the opioids inhibit pain by binding to these receptors isn’t fully understood. Opioids may be potent painkillers, but their overuse comes with the spectre of opioid addiction. Excessive use leads to over-stimulation of the brain’s ‘reward’ pathways; the brain also tries to compensate by reducing the number of opioid receptors, meaning progressively more of the opioid is required to achieve the same highs. No single treatment is effective for all opioid dependent patients, and oddly enough, some of the opioids drugs are used in some treatments. Methadone and buprenorphine are both commonly prescribed, as they are longer acting than, for example, heroin, and so allow for less frequent dosing. Tolerance is also slow to develop, and as such their use has been associated with a reduction in the use of other opioids in opioid dependent individuals. Although fentanyl is the most potent opioid shown on the chart, more powerful opioids do exist. The most potent used in humans is sufentanil, considered to be approximately 500-1000 times stronger than morphine. Carfentanil, with a potency considered to be around 10,000 times that of morphine, is used as a general anaesthetic in large animals.

Paracetamol is something of an oddity among the painkillers, in that it’s categorized separately, rather than in one of the two main groups. Part of the reason behind this is that we still don’t have a very good idea of how paracetamol exerts its painkilling effects. It’s thought that, like the NSAIDs, it works by inhibiting cyclooxygenase enzymes, but there are also suggestions that it works on the endocannabinoid system in the body, which plays a part in pain. In short, we still don’t really know how it functions. Paracetamol also has a detraction, in that its toxic dose is relatively close to the effective dose. Excessive use or overdose can lead to damage to cells in the liver, which can in turn lead to liver failure and death.

(Source: Compound Interest).

[brainsandbodies]

Coloured X-ray of a sagittal section through a human skull. “The skull has been sliced in half down the centre, revealing details of the internal structures. These include the delicate bones and spaces of the paranasal sinuses (around the nose and eyes, centre left). The fused bones of the cranium encase and protect the brain. 

The nasal, cheek and upper jaw bones are fused to the cranium to form the facial skeleton (left). The lower jaw bone (mandible, lower left), is attached at flexible joints, allowing it to move. The upper and lower jaw bones contain 32 permanent teeth (lower left). The eye sockets (one at far left) house the eyes.” Credit: D. Roberts

Text: Daily Anatomy

[jewsee-medicalstudent]

Addison’s Disease.

Addison’s disease is a rare but known disorder (John Fitzgerald Kennedy suffered from it) and it is also referred to as adrenal insufficiency. Adrenal insufficiency develops when adrenal glands do not produce enough of the hormone cortisol. This can happen due to a problem within the adrenals (called Addison’s disease or primary adrenal insufficiency) or due to a problem with ACTH, the signal the brain sends to the adrenals instructing them to make cortisol (called secondary adrenal insufficiency).

An important distinction for patients is that people with primary adrenal insufficiency (Addison’s disease) usually don’t make enough of the hormone aldosterone too; so in addition to taking cortisol replacement, they also need aldosterone replacement. Also, ACTH levels are elevated. People with secondary adrenal insufficiency are only low on cortisol. 

Causes: Primary adrenal insufficiency - the outer layer of the adrenal glands is called the adrenal cortex. If the cortex is damaged, it may not be able to produce enough cortisol. A common cause of primary adrenal insufficiency is an autoimmune disease that causes the immune system to attack the adrenal gland(s). There are some very rare syndromes (several diseases that occur together) that can cause autoimmune adrenal insufficiency, such as Autoimmune Polyendocrine Syndrome (type 1 or type 2). Other causes include: amyloidosis; bleeding into the adrenal glands; cancer that spreads to the adrenal glands; infections (bacterial, fungal, tuberculosis) of the adrenal glands; surgical removal of the adrenal glands. Secondary adrenal insufficiency - it is caused by a lack of ACTH, made in the pituitary gland. By far the most common cause of this type of adrenal insufficiency is chronic steroid use.

Signs and symptoms: 

Weakness

Fatigue

Abdominal pain

Nausea

Weight loss

Low blood pressure

Increased pigmentation of the skin, including areas not exposed to the sun (due to high levels of ACTH in primary adrenal insufficiency. This occurs because melanocyte-stimulating hormone (MSH) and ACTH share the same precursor molecule, pro-opiomelanocortin (POMC))

Salt craving (due to low levels of aldosterone in primary adrenal insufficiency)

Postural Hypotension

Depression

Treatment: it involves replacing the cortisol and/or aldosterone that the body is not able to produce, or that it secretes in an insufficient quantity. Cortisol is replaced with an oral synthetic glucocorticoid. The drug is taken one or two times each day. Aldosterone is replaced with an oral mineralcorticoid.

[bersiker]

Our white blood cells attacking a parasite.

[radiopaedia]

Radiologists aren’t the only ones who see things!

Via @aukeappelman on Twitter

[fuckyeahnarcotics]

A patient with sustained monomorphic ventricular tachycardia. 

[inthewards]

Overlap Syndrome

Dermatomyositis overlaps with systemic sclerosis and mixed connective tissue disease

Signs:

Sclerotic thickening of dermis

Contractures

Esophageal hypomotility

Microangiopathy

Calcium deposits

[inthewards]

Lupus Nephritis

Systemic lupus erythematosus is an autoimmune multisystem disorder with a remitting and relapsing course. There is a strong female to male prepondance (9:1). The onset is usually in the 2nd/3rd decade of life, however it can occur at any age.

Hypersensitivity:

Type 2: Cytotoxic, Antibodies against cells

Type 3: Immune complex deposition in organs

Involves an array of bewildered antibodies:

Antinuclear antibody: Sensitive (+ve in 95% SLE patients)

Anti-dsDNA: Specific for SLE, can be used to monitor disease activity (high levels)

Anti-Sm antibody: Specific for SLE

Anti-phospholipid antibody

Monitoring SLE disease activity:

Anti-dsDNA: high 

Serum complement: low C3 and C4, high C3 degradation product

ESR: high / do CRP to distinguish lupus flare from infection

Renal involvement is common and can exacerbate renal failure which can lead to death. WHO has classified into classes of lupus nephritis

WHO Classification:

Class I  (rare)

Minimal Mesangial Lupus Glomerulonephritis

Light microscope: histologically normal

Electron microscope: mesangial deposits

Renal failure is rare

Class II  (20%)

Mesangial Proliferating Lupus Nephritis

Mild clinical symptoms

Responds to corticosteroids

Renal failure is rare

Class III  (25%)

Focal Proliferative Lupus Nephritis

Responds to high dose corticosteroids

Mild microscopic haemturia and proteinuria

<50% glomeruli affected

Renal failure is uncommon

Class IV  (50% - common)

Diffuse Proliferative Lupus Nephritis

Most serious form 

Haematuria + moderate to severe proteinuria

Hypertension

Renal insufficiency / renal failure is common

Glomerular injury eventually gives rise to glomerulosclerosis

Class V  (15%)

Membranous Lupus Nephritis

Severe proteinuria and nephritic syndrome

Extreme edema

Microscopy shows widespread thickening of capillary wall 

Class VI  

Advanced Sclerosing Lupus Nephritis

>90% of glomeruli sclerosed

[inthewards]

Allopurinol

Allopurinol is a xanthine oxidase inhibitor Indications for rx in patients with gout: - Recurrent attacks >3 times per year - Chronic tophaceous gout - Uric acid nephropathy - Persistently high uric acid levels - Prophylaxis to treatment that can exacerbate acute gout Medical uses: - Gout and hyperuricaemia - Tumour lysis syndrome - Renal diseases - Hypertension Side-effects - Stevens Johnson Syndrome - Toxic epidermal necrolysis - Diarrhoea - Thrombocytopenia - Leukopenia - Allopurinol hypersensitivity syndrome : erythematous rash, fever, hepatitis, hypereosinophilia, renal failure

[medicowesome]

Hello.

Prolactin is pro-lactation hormone. It aids in breast development during pregnancy and milk secretion from the breast during nursing.

It’s regulation is kind of complex which is why we’ll be learning about it today. I’ll also be sharing a few mnemonics that will help you remember these...

[inthewards]

Modes of Delivery: NVD + Instrumental

Normal vertex delivery

Always aim for NVD where possible

Good descend

No signs of obstructed labour

Not >3/5 of head above abdomen

Instrumental delivery

Indications:

Prolonged 2nd stage of labour (Nullip: >2hours, 3hours if on epidural, Multip: >1hour, 2hours if on epidural)

Fetal distress: Cord accidents, placental insufficiency

Maternal distress: Exhaustion, maternal disease: Cardiovascular/neuro diseases

Prophylaxis: Preterm labour, malpositions, after coming head in breech delivery

Conditions: (MNEMONIC: FORCEPS)

F - Favourable presentation (Vertex, face, after coming head in breech delivery

O - Os full

R - Ruptured membranes

C - Contractions present + consent taken

E - Engaged, empty bladder and bowel

P - Placenta praevia exlcuded, position known (OA)

S - Sterile

Preparation:

Lithotomy position

Aseptic technique - Drape and clean vulva 

Anaesthesia - local infiltration / pudendal block

Empty bladder 

Resuscitation facilities for neonate present

Contraindications:

Potential for unacceptable fetal risk

Prematurity

Fetal abnormalities (eg. Osteogenesis imperfecta)

Fetal bleeding diathesis

Inexperienced operator + inadequate facilities

Complications:

Maternal:

Laceration

Trauma

Haemorrhage

Fetal:

Intraventricular haemorrhage

Cerebral palsy

Bruises and forceps marks

Skull fracture

Facial nerve palsy

Types of Forceps:

Neville-Barns Forceps

Mid-cavity forceps

Engaged head

Leading part of head below ischial spines (Station +2)

Indications: Cephalic OA, OP position, face malpresentation, after coming head in breech

Simpsons Forceps

Low forceps

> station +2

Wriggley's Forceps

Crowning, head visible at introitus

Outlet forceps

Kielland's Forceps

Rotational forceps

Used for rotation and extraction of fetal head arrested in deep OP or transverse

No pelvic curvature

Vacuum

Cannot be used for preterm labour, caesarean section, after coming head in breech

Allows rotation in malposition

Conditions to use are same as forceps, however Os not necessarily need to be fully dilated (>8 sufficient)

Only vertex presentation

Kiwi suction cup

Single use only

Pa: 0.7 - 0.8kg/m2

Malpositions of fetal head can be corrected and auto-rotation can occur naturally

Apply cup at posterior fontanelle

Ventouse suction cup

2 types: Metal or silicon cups

External pump

Pa: 0.7 - 0.8kg/m2

Posterior cup

Complications

Maternal:

Lacerations

Fetal:

Severe chignon

Intracranial haemorrhage

Separation of skull bones, skull fracture

Cephalohaematoma

Tentorial tears

Scalp necrosis

[inthewards]

Pain Relief in Labour

Entonox (Laughing gas)

Opioids (Pethidine, fentanyl)

Emotional support

Complementary therapy (Aromatherapy)

Epidural

Epidural

Procedure explanation:

Epidural pain relief on of the most effective and reliable ways to relieving labour pain

Needle inserted near your back bone into the spinal canal

Plastic tube will be put in place to deliver pain relief medication

Expectations:

Complete pain relief cannot be guaranteed as different women respond differently

Effective pain relief is balanced against side effects

Some degree of pain may still be felt especially near the time of delivery of baby

Benefits:

Safe and consistently reliable

Placenta and baby may get better blood flow in between and during contractions

Reduces stress related responses of the body to pain

Beneficial for women with hypertension, pre-eclampsia, heart problems

Side effects:

Common

Loss of feeling - numbness to legs/lower body, loss of bladder sensation

Muscle weakness - goes away as medication wears off

Shivering

Nausea & vomiting

Itch

Fever - if more than 38deg celcius, suspect infection

Effects on baby: decreased heart rate (can be treated with fluids and medication)

Bruising+ backache

Paraesthesia

Uncommon

Spinal headache: occurs in 1% of women, pain in forehead, posterior of head and neck, worsened in upright position, can be treated with spinal analgesia

Analgesia failure: inadequate analgesia given, suboptimal placement of needle, migration of needle out of spinal canal, inadequate time for analgesia to work, disconnection

Rare

Infection (spine and brain)

Spinal injury / lesions

Respiratory depression

Convulsion

Wrong placement

[inthewards]

Oxytocin in Obs/Gyn

Syntocinon:

Synthetic oxytocin

Used for: Induction of labour, stimulating labour, postpartum haemorrhage control

Given IV

Ergometrine:

Ergoline derivatives + primary ergot + morning glory alkaloids

Used for: facilitate delivery of placenta, control postpartum haemorrhage

Given IV

Syntometrine: 

Syntocinon + Ergometrine

Given IM

Syntometrine & Ergometrine: causes hypertension which can lead to stroke/seizures

Contraindications: >40 year old, hypertension, smoker, pre-eclampsia, pregnancy induced hypertension, renal diseases, cardiovascular diseases, arrhythmias

Use IV Syntocinon if syntometrine and ergometrine contraindicated

Prophylaxis for postpartum haemorrhage:

Blood group and cross match

Give syntometrine/syntocinon upon delivery of anterior shoulder

[inthewards]

Pre-eclampsia / Eclampsia

Risk factors:

>35 year old

Primip

Multiple pregnancies

Molar pregnancies

Pregnancy induced hypertension (PIH)

Previous PIH

Family Hx of PIH

Pre-existing hypertension, renal disease, autoimmune disease

Hx should include:

When was the diagnosis of pre-eclampsia, what was the treatment, compliance to treatment, ongoing monitoring

Sxs - headache, blurry vision, epigastric pain, nausea (signs of impending eclampsia)

Fetal movements?

Per vaginal bleed?

Growth of fetus / AFI scans / fetal scans till date

Current gestational age

Physical Examination:

General - Vital Signs! Height, weight (look out for trend increase), pallor, petechiae, edema

Lungs - crepitations sec. to pulmonary edema

Abdomen - SFH, liquor volume, obvious fetal movements, scars, estimated fetal weight, woody hard uterus - indicative of placenta abruptio

Neuro - Hyperreflexia, clonus

Fundoscopy - hypertensive changes

Investigations:

- Urine dipstick, 24 hour urine collection (albumin measure)

- FBC - Hb (anaemia), Platelets (low? <100)

- U/E/Cr - Renal function / metabolic derangements? / 

- Uric acid

- LFT - Look at AST / ALT (elevated > x2?)

- GXM - blood group and cross match

- Ultrasound - Estimated fetal weight, amniotic fluid index

Management

For mild to moderate pre-eclampsia, monitor closely as outpatient.

Counsel patient: what is pre-eclampsia, dangers of pre-eclampsia, can be cured via delivery, return of BP to normal within 6 weeks post partum

Pharmaco: methyldopa to control hypertension

Monitor: Blood pressure, Urine dipstick, keep a diary

Discuss about sxs of impending eclampsia - headache, blurry vision, epigastric pain, nausea - to come to hospital immediately, or if blood pressure uncontrollable, increasing trend in proteinuria

Follow-up: weekly! - BP measurement, urine dipstick, fetal ultrasound, physical examination

Re-assure patient

For severe eclampsia

ADMIT PATIENT

CALL FOR HELP - Senior Obs/MO/Registrar, Labour room sisters, Anaesthetist/Operating theatre (Emergency LSCS)

Start Pre-eclampsia chart (Vitals - BP/PR, Weight, edema, urinary albumin levels, fetal movement/HR, input/output chart)

CTG - monitor baby

Anti-hypertensives : methyldopa (slow acting) / Hydralazine (fast acting) - be careful of quick drop in BP. Provide IV fluids if BP dropping too quickly. Do not give fluids if evidence of pulmonary edema

Seizure prophylaxis: MgSO4 ! S/e: palpitations, hypotension, flushing, sweating. Toxicity: Renal failure, respiratory depression, hyporeflexia. Antidote: Calcium gluconate. Monitor Levels! 

Plan for delivery: LSCS vs Normal vertex delivery. Indications for delivery: fetal compromise (abnormal CTG, abnormal doppler, IUGR, AFI <5), maternal compromise (placenta abruptio, end-organ damage - oliguria, HELLP syndrome, signs + sxs of impending eclampsia), dexamethasone, 

Intrapartum - continue MgSO4 till 24hours postpartum (14% seizures can occur postpartum), control BP, LSCS if fetal compromise

Postpartum - monitor resolution of blood pressure, monitor renal function and resolution of biomarkers (LFTs, FBC - platelets), refer physician if still hypertensive and/or proteinuria

Counsel - reoccurrence in subsequent pregnancies. if severe pre-eclampsia, 30% can reoccur in future pregnancies