Sandbox:AyeshaFJ

Cardiovascular Disorders and COVID-19

Out of hospital SCD

Pathophysiology

• Drug induced:

Since the COVID-19 pandemic, several pharmacological therapies have been proposed, one of them is of two anti-malarial and antirheumatic drugs called Chloroquine or Hydroxychloroquine. Due to their cost-effectiveness and easy availability, there is a surge in the use of Chloroquine and Hydroxychloroquine, with or without Azithromycin. The clinical trials in order to estimate their efficacy are still in the preliminary stage, however, a notable concern is of their cardiac adverse effects. This includes QT prolongation and Torsade de pointes (TdP) leading to sudden cardiac death. The risk is there when these drugs are prescribed separately, however it increases several folds when these drugs are administered together, especially in patients with underlying hepatic disease or renal failure.

• Genetic susceptibility:

Epidemiological studies have shown that African Americans have higher COVID-19 associated morbidity and mortality as compared to people from other ethnic groups. Recent studies show that this ethnic predilection is due to the genetics factors which contribute to a common ion channel variant p.Ser1103Tyr-SCN5A which confer an increased risk of drug-induced long QT syndrome (DI-LQTS) and drug-induced sudden cardiac death (DI-SCD). p.Ser1103Tyr-SCN5A generates late or persistent sodium current which is further aggravated by hypoxia or respiratory acidosis secondary to lungs involvement in COVID-19. This has and has been linked to an increased risk of ventricular arrhythmia (VA) such as torsade de pointes and sudden cardiac death (SCD) in African Americans

Spontaneous coronary dissection

Pathophysiology In patients with an inflammatory overload, a localized inflammation of the coronary adventitia and periadventitial fat can occur. This could lead to the development of sudden coronary artery dissection in a susceptible patient. Signs and symptoms Treatment

Neurofibromatosis

Neurofibromatosis 1

Neurofibromatosis 2

NF1 tumor suppresor gene Mutation located on chromosome 17, encodes for neurofibromin

NF2 tumor suppresor gene Mutation located on chromosome 22, encodes for merlin

clinical features: Cafe-au-lait spots, multiple neurofibromas and lisch nodules

Clinical features: bilateral acoustic neuromas

Features of Wenicke-Korsakoff Syndrome
Associated conditions	Chronic alcoholism (most common). Malnutrition.
Pathophysiology	Thiamine deficiency impairs ATP generation leading to neuronal dysfunction and death. It mostly has paraventricular lesions involving mammillary bodies and dorsomedial bodies.
Clinical findings	Confusion. Oculomotor dysfunction (horizontal nystagmus and bilateral abducens palsy) Postural and gait ataxia. Memory impairment (permanent).
Treatment	Intravenous thiamine. Administration of glucose before the thiamine can worsen the symptoms.

Acne vulgaris
Clinical features	Comedonal acne:Closed or open comedones on forehead, nose and chin. Inflammatory acne: Small, erythematous papules and pustules. Nodular acne: Large painful nodules; sinus tracts and scarring.
Pathogenesis	Hyperkeratinization and obstruction of the pilosebacous follicles. Sebaceous gland enlargement and increased sebum production. Metabolism of sebaceous lipids by Cutibacterium acnes and release of inflammatory fatty acid. Follicular inflammation and rupture,
Risk factors	i) Increased circulating androgen (e.g. PCOS, puberty) ii) Mechanical trauma/friction (excessive scrubbing, tight clothing) iii) Comedogenic oil based skin and hair products. iv) Excessive heat. v) Obesity

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Criteria for the diagnosis of SLE
Clinical features	Characteristics
1)Malar rash	Fixed erythema, flat or raised, sparing the nasolabial folds
2)Discoid rash	Erythematous raised patches with adherent keratotic scarring and follicular plugging.
3)Photosensitivity	Rash due to unusual reaction to sunlight.
4)Oral ulcer	Oral or nasopharyngeal ulcers, which may be painless.
5)Arthritis	Non-erosive arthritis, involving >2 peripheral joints.
6)Serositis	Pleuritis or pericarditis
7)Renal disorder	Persistent proteinura ( >0.5g/24hrs) or cellular casts (red cell, granular or tubular).
8)Neurological disorder	Seizure or psychosis, in the absence of provoking drugs or metabolic derangement.
9)Hematological disorder	Haemolytic anemia or leucopenia (<4 x109) or lymphopenia (<1x109) or thrombocytopenia (<100x109) in the absence of offending drugs.
10)Immunological	Abnormal titre of Anti-DNA antibodies or presence of Sm antigen or positive antiphospholipid antibodies.
11)Anti-nuclear Antibody (ANA)	Abnormal ANA titre measured by immunofluorescence
Diagnosis of SLE is made in an adult if 4 out of 11 features are present either serially or simultaneously.

• Erythematous raised patches with adherent keratotic scarring and follicular plugging.

Congenital anomalies of the urinary system

Kidneys

Renal pelvis

Ureter

Renal agenesis

Duplication of renal pelvis

Duplication of ureter

Renal ectopia

Congenital megaureter

Horseshoe kidney

Post-caval ureter

Unilateral fusion

Ureterocele

Congenital cystic kidney

Infantile polycystic kidney

Unlilateral Multicystic Kidney

Simple cyst of the kidney

Aberrant renal vessels

T

Mycosis fungoides

Stage IA-IIA

Stage IIA

Stage III

Stage IV

• Expectane policy • Topical steroides [IV-A] • nb-UVB[III,A] • PUVA [III-A] • Topical mechlorethamine [II,B] • Local RT [IV,A]

• Skin direct therapy(SDT) + local radiotherapy • ST[III+A] • (SDT+) retiods[III,B] • (SDT+) IFN a {III,B] • TSEBT [III,A]

• (SDT+) retinoides • (SDT+) IFNa • ECPI INFa +/- rtinoides • Low dose MTX • [IV-B]

• Gemcitabine • Liposomal doxorubicin • Brentuximab vedotin[II,B]

• (SDT+) retinoides [III,B] • (SDT+) IFNa [III,B] • Retinoides +IFN a [II,B] • TSEBT [IV,A]

• Gemcitabin [IV,B] • Liposomal doxorubicin [IV,B] • Brentuximabvedotin [II,B] • Combinatio Cht [Iv,B] • AlloSCT[V,C]

TSEBT[LV,B]

• Combination Cht [IV,B] • AlloSCT [V,C]