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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]