Acute pancreatitis

 

Benign Prostatic Hyperplasia

Growth chart - Head circumference-for-age & Weight-for-lengths: Girls, birth to 36m

Growth chart - Head circumference-for-age & Weight-for-lengths: Boys, birth to 36m

Growth chart - Lengths-for-age & Weight -for-age percentiles: Girls, birth to 36m

Growth chart - Lengths-for-age & Weight -for-age percentiles: Boys, birth to 36m

Growth Chart - BMI-for-age percentiles: Girls, 2 to 20y

Growth Chart - BMI-for-age percentiles: Boys, 2 to 20y

Growth Chart - Stature-for-age percentiles: Girls, 2 to 20y

Growth Chart - Stature-for-age percentiles: Boys, 2 to 20y

Growth Chart - Weight-for-age percentiles: Girls, 2 to 20y

Growth Chart - Weight-for-age percentiles: Boys, 2 to 20y

Growth chart - Head circumference-for-age: Girls, birth to 36m

Growth chart - Head circumference-for-age: Boys, birth to 36m

Growth chart - Lengths-for-age percentiles: Girls, birth to 36m

Growth chart - Lengths-for-age percentiles: Boys, birth to 36m

Growth chart - Weight-for-age percentiles: Girls, birth to 36m

Growth chart - Weight-for-age percentiles: Boys, birth to 36m

Vesicoureteral Reflux (VUR)

Definition

Vesicoureteral reflux (VUR) is an abnormal movement of urine from the bladder into ureters or kidneys. Urine normally travels from the kidneys via the ureters to the bladder. In vesicoureteral reflux the direction of urine flow is reversed (retrograde).

Causes

·         Primary VUR

Insufficient submucosal length of the ureter relative to its diameter causes inadequacy of the valvular mechanism.

·         Secondary VUR

Valvular mechanism is intact.

But, overwhelmed by raised vesicular pressures associated with obstruction, which distorts the ureterovesical junction.

Futher divided into:

1.      Anatomical: Posterior urethral valves; urethral or meatal stenosis.

These causes are treated surgically when possible.

2.      Functional: Bladder instability, neurogenic bladder and non-neurogenic neurogenic bladder urinary tract infections may cause reflux due to the elevated pressures associated with inflammation.

Resolution of functional VUR will usually occur if the precipitating cause is treated and resolved. Medical and/or surgical treatment may be indicated.

International Classification of Vesicoureteral Reflux

Grade I – reflux into non-dilated ureter

Grade II – reflux into the renal pelvis and calyces without dilatation

Grade III – mild/moderate dilatation of the ureter, renal pelvis and calyces with minimal blunting of the fornices

Grade IV – dilation of the renal pelvis and calyces with moderate ureteral tortuosity

Grade V – gross dilatation of the ureter, pelvis and calyces; ureteral tortuosity; loss of papillary impressions

Diagnosis

The following procedures may be used to diagnose VUR:

1.      Nuclear cystogram (RNC)

2.      Fluoroscopic voiding cystourethrogram (VCUG)

3.      Ultrasonic cystography

4.      Abdominal ultrasound

Classification of Venous Diseases

CEAP classification

The elements of the CEAP classification are:

	Clinical severity
	Etiology or cause
	Anatomy
	Pathophysiology

 There are seven grades of increasing clinical severity:

Grade	Description
C 0	No evidence of venous disease.
C 1	Superficial spider veins (reticular veins) only
C 2	Simple varicose veins only
C 3	Ankle oedema of venous origin (not foot oedema)
C 4	Skin pigmentation in the gaiter area (lipodermatosclerosis)
C 5	A healed venous ulcer
C 6	An open venous ulcer

Recommendations for new patients with venous disease

Group	Action
CEAP 1	No need to refer to NHS clinic, cosmetic problem only
CEAP 2	Refer routinely to "Fast Track Varicose Vein Clinic" for photoplethysmography assessment
CEAP 3 - 5	Refer soon to "Fast Track Varicose Vein Clinic" for venous duplex ultrasound assessment
CEAP 6	Refer urgently to "One Stop Leg Ulcer Clinic" for full leg ulcer assessment

Acute Limb Ischaemia (ALI)

 Rutherford's Classification of Peripheral Arterial Disease

Class	Category	Prognosis	Sensory loss	Muscle weakness	Arterial Doppler	Venous Doppler
I	Viable	No immediate limb threat	None	None	Audible	Audible
IIA	Threatened: marginal	Salvageable if treated promptly	Minimal-none	None	+/-Audible	Audible
IIB	Threatened: Immediate	Salvageable if treated immediately	More than just toes	Mild-moderate	Rare audible	Audible
III	Irreversible	Limb loss or permanent damage	Profound	Profound	None	None

-from the Society of Vascular Surgery/International Society of Cardiovascular Surgery (Rutherford et al, 1997)

1.      Usually thrombotic occlusions are class I or IIA and are treated with intra-arterial thrombolysis if symptom duration <14 days (especially if bypass graft occlusion) and if patient has significant co-morbidities/high operative risk.

2.      Usually embolic occlusions are class IIB or III.  They usually require surgery as thrombolytics take effect too slowly.

Contraceptions

Menopause

Vulvovaginitis

Sexually Transmitted Disease

Vulva Cancer

Ovarian Cancer

Gestational Trophoblastic Disease (GTD)

Endometrial Cancer

Endometriosis

Cervical Intraepithelial Neoplasia (CIN)

Cervical Cancer

Benign Ovarian Tumour

Benign Disease of Uterus & Cervix

Assisted Conception

Infertility

Polycystic Ovarian Syndrome (PCOS)

Ectopic Pregnancy

Miscarriage

Hyperemesis Gravidarum

Menorrhagia

Dysmenorrhoea

Dysfunctional Uterine Bleeding (DUB)

2' Amenorrhoea

Anti-Arrhythmic Agents

Singh Vaughan Williams classification of antiarrhythmic agents

1.       Class I agents interfere with the sodium (Na⁺) channel.

2.       Class II agents are anti-sympathetic nervous system agents.

Most agents in this class are beta blockers.

3.       Class III agents affect potassium (K⁺) efflux.

4.       Class IV agents affect calcium channels and the AV node.

5.       Class V agents work by other or unknown mechanisms.

Class	Known as	Examples	Mechanism
Ia	Na+ channel blockers	Quinidine Procainamide Disopyramide	(Na+) channel block (intermediate association/dissociation)
Ib		Lidocaine Phenytoin Mexiletine	(Na+) channel block (fast association/dissociation)
Ic		Flecainide Propafenone Moricizine	(Na+) channel block (slow association/dissociation)
II	Beta-blockers	Propranolol Esmolol Timolol Metoprolol Atenolol Bisoprolol	beta blocking Propranolol also shows some class I action
III	K+ channel blockers	Amiodarone Sotalol Ibutilide Dofetilide E-4031	K+ channel blocker Sotalol is also a beta blocker[2]
IV	L-type Ca2+ channel blockers	Verapamil Diltiazem	Ca2+ channel blocker
V	Miscellaneous	Adenosine Digoxin	Work by other or unknown mechanisms (Direct nodal inhibition).