RTR-INTERNAL

MEDICINE
CASE PRESENTATION
Tabajonda, Raphael Adrian M. MD
POST GRADUATE INTERN
GENERAL OBJECTIVES
-broaden the knowledge of its
audience about HYPERTHYROID
HYPOKALEMIC PERIODIC PARALYSIS;
 NATURE,
 RISK FACTORS
 EPIDEMIOLOGY,
 PATHOGENESIS,
 CLINICAL MANIFESTATIONS
 TREATMENT AND PROGNOSIS
DATE OF INTERVIEW: OCTOBER 12,
2018
SOURCE OF INFORMATION:
PATIENT
RELIABILITY: 95%
• A case of J.J
• MALE
• 25 years old
• born on MAY 25, 1993
• single
• Roman Catholic
• Filipino

GENERAL INFORMATION
LOWER EXTREMITIES
WEAKNESS
CHIEF COMPLAINT
History of
present illness:
- (+) WEAKNESS OF BOTH
LOWER EXTREMITIES
- (-) DYSPNEA
- (-) NAUSEA
- (-) VOMITING
- (-) CHESTPAIN
- (-) ABDOMINAL PAIN
1 week PRIOR - (-) URINARY SYMPTOMS
TO ADMISSION (x) NO MEDICATIONS WERE
TAKEN
(x) NO CONSULT WAS DONE
History of
present illness:
 WEAKNESS PROGRESSES
 NAUSEA
 DIFFICULTY IN AMBULATION
 FELL SEVERAL TIMES WITH
ABRASION TO THE KNEE
2 DAYS PRIOR • CONSULT WAS DONE AT
TO ADMISSION DISTRICT HOSPITAL
History of
present illness:
• CONSULT WAS DONE
• LABS WERE REQUESTED
• DECREASE IN POTASSIUM
NOTED < 2.5mmol/l
• Patient refused for
admission
2 DAYS PRIOR • Was given celecoxib for
TO ADMISSION pain and KCL tab 2x a day
for hypokalemia
History of
present illness:
- (+)WORSENING OF
SYMPTOMS PROMPTED
CONSULT
- ADMITTED

1 DAY PRIOR
TO ADMISSION
PAST MEDICAL HISTORY

 With allergies to ALCOHOLIC BEVERAGES

 Pediatric Illnesses: NONE
 Medical: none
 Surgical: none
 Psychiatric: none
FAMILY HISTORY

 Father 48 years old apparently well

 Mother 47 years od apparently well
 Patient claims that she had close relatives with HYPERTENSION,
DIABETES, ASTHMA, AND KIDNEY DISEASE
PSYCHOSOCIAL HISTORY

 Smoker
 Alcoholic beverage drinker.
REVIEW OF SYSTEMS

 GENERAL: (+) body weakness, no weight loss since onset of illness, no

fever, no fatigue
 SKIN: no itchiness, sores, lesions, pallor, no rashes
 HEAD: no headache, no lightheadedness, dizziness
 EYES: no pain, redness, blurring of vision or excessive tearing
 EARS: no tinnitus, no discharges
 NOSE AND SINUSES: no nasal stuffiness, no watery discharges, no itching,
no epistaxis
REVIEW OF SYSTEMS

 MOUTH AND THROAT: dry throat, no hoarseness, no

bleeding gums
 NECK: no pain, no rigidity, no lumps
 RESPIRATORY:no productive cough, no dyspnea,
orthopnea, hemoptysis
 CARDIOVASCULAR: no chest pains, palpitations
 REVIEW OF SYSTEMS

GIT: poor appetite, nausea, vomiting, defecates at least once a day with a
stool brownish in color, and soft in consistency
GUT: no hematuria, dysuria, polyuria, oliguria, urinates at least 4-5 times a
day, yellow in color and amounting to 200 ml per urination.
MUSCULOSKELETAL: muscle weaakness
HEMATOLOGIC: no easy bruising
ENDOCRINE: no excessive thirst/hunger, no heat/cold intolerance
PSYCHIATRIC: no nervousness, tension, memory loss
PHYSICAL EXAMINATION

General Survey
Patient was examined conscious, coherent, oriented as to time, place and person,
cooperative, mesomorph, afebrile, not in cardio-respiratory distress, with the
following vital signs:

BP 120/70 mmHg
HR 79 bpm
RR 23 cpm
TEMP 36.1 C
PHYSICAL EXAMINATION

INTEGUMENT
Skin: dry, warm, brown complexion, no scars, good skin turgor, no jaundice, no edema, no
ecchymoses

Nails: good capillary refill, no clubbing, no cyanosis

HEAD
Hair: short, black, fine, evenly distributed on scalp
Scalp: no tenderness, no scars, no active lesions
Skull: normocephalic, atraumatic
PHYSICAL EXAMINATION

EYES:
Eyebrows: symmetrical, fine, black, no active lesions
Eyelashes: fine, black, oriented outwards
Eyelids: no edema , no sty, no lid lag
Conjunctiva: pinkish palpebral conjunctiva
Sclera: anicteric, no hemorrhage
Cornea: no opacities, no ulceration
Pupils: symmetrical, 2mm in diameter, reactive to direct & consensual light
stimulation
EOM: full
PHYSICAL EXAMINATION

EARS: symmetrical, no discharges, no active lesions, no impacted cerumen

NOSE: no colds, no septal deviation, no epistaxis, no nasal flaring

MOUTH & THROAT:

Lips: pinkish, no angular deviations, no cold sores
Mucous membrane: moist, pinkish, no bleeding, no sores
Gums: pinkish, no bleeding
Tongue: pinkish, no ulceration
Throat: uvula at midline, no inflammation
PHYSICAL EXAMINATION

NECK: trachea at midline, thyroid gland moves with deglutition, supple, no

palpable lymph nodes
CHEST & LUNGS:
Inspection: truncal in shape, symmetrical lung expansion, no lagging
Palpation: confirmed symmetrical lung expansion, unimpaired tactile fremitus at
all lung fields
Percussion: resonant in all lung fields
Auscultation: bronchovesicular breath sounds over all lung fields, no crackles, no
rales, no wheezing, no pleural friction rub
PHYSICAL EXAMINATION

HEART:
Adynamic precordium, regular rhythm synchronous with radial pulse, no
murmurs, no pericardial friction rub
ABDOMEN:
Inspection: full, symmetrical, no visible peristalsis, no visible veins
Palpation: no tenderness, spleen & kidney not palpable,
Percussion: tympanitic , no fluid wave
Auscultation: normoactive bowel sounds, no bruit, no peritoneal friction
rub
PHYSICAL EXAMINATION

EXTREMITIES:
Inspection: equal length, no deformities, no active
lesions, no edema,
Palpation: no muscular tenderness
BACK AND SPINE:
Inspection: no abnormal deviation, no muscle wasting
Palpation: no tenderness or mass
NEUROLOGIC EXAMINATION

 MENTAL STATUS EXAM: active and

coherent
 CRANIAL NERVES:
 CN I: (coffee) no anosmia
 CN II & III: pupils 4 mm in diameter,
symmetrical, reactive to direct and
consensual light stimulation,
NEUROLOGIC EXAMINATION

 CN III, IV, VI: able to move eyes

upward, downward, medially and
laterally
 CN V: patient able to feel and
recognize sharp and dull object
pressed against the skin on either
side of the body, positive sensory
function to pain and touch, positive
corneal reflex
 NEUROLOGIC EXAMINATION

 CN VII: able to smile, able to frown,

symmetrical upon crying
 CN VIII: responsive to verbal stimuli
 CN IX and X: gag reflex, able to swallow
 CN XI: able to turn head to both sides
against resistance, shrugs
 CN XII: protrude tongue, deviation to
L/R
NEUROLOGIC EXAMINATION

 Motor:
 3/5 = LOWER EXTREMITIES
5/5 5/5

 DTR:
PATELLAR & ACHILLES= HYPOACTIVE

 SENSORY:
3/5 3/5
 100 % INTACT
NEUROLOGIC EXAMINATION

 Cerebellum
 - able to perform pronation-
supination
 VII. Meninges
 (-) nuchal rigidity
 (-) Kernig’s sign
 (-) Brudzinski sign
 VIII. ANS (-) excessive sweating
SALIENT FEATURES
• 25 years old
• male
• Asian
• Chief complaint: lower
extremities weakness
• Alcoholic
• Hypokalemia: < 2.8mg/dl
• Took KCL tab 2x a day
• Motor : 3/5 both lower
extremities
• Nausea
Differential diagnosis
Pivot : paraparesis
Infectious: Transverse myelitis

Rule in Rule out

progressive muscle weakness of the
lower extremities
(-)radicular pain
(-)hyperreflexia
(-)bladder symptoms
(-)neurological(CNS) infections
(-)point tenderness in the spine
Degenerative : Amyotropic lateral
sclerosis
Rule in Rule out
progressive muscle weakness of the (-) slurring of speech
lower extremities (-)trouble swallowing
(-) hyperreflexia
Degenerative : myasthenia gravis

Rule in Rule out

progressive muscle weakness of the (-)droopy eyelid
lower extremities (-) double vision
(-) dysphagia
(-) slurred speech
(-) muscle pain in the neck
Final impression

 THYROTOXIC HYPOKALEMIC PARALYSIS

Course in the ward
At the ER ( OCT 12,2018)

 Patient was given with PLR 500ml + 20meqs KCL at 1-gtts/min:

 Diagnostics requested:
 Potassium, Sodium
 CBC with platelet count
 12L ECG, BUN, Creatinine
 TSH,FT4,FT3
 Urinalysis
 Chest xray PA view
 Ultrasound of the abdomen
laboratories
October 12, 2018 4:58PM
HEMATOLOGY
TEST RESULTS UNIT NORMAL VALUES
COMPLETE BLOOD COUNT
WBC Count 6.5 X10^10g/L 5.0 – 10.0
Hemoglobin 155 g/L 140 – 180
Hematocrit 0.48 g/L 0.40 – 0.54
Platelet Count 348 X10^10g/L 150 – 450
DIFFERENTIAL COUNT
Neutrophils (%) 54 % 50 – 70
Lymphocytes (%) 37 % 20 – 40
Monocytes (%) H9 % 0–7
 October 12, 2018 3:36 PM
ARTERIAL BLOOD GAS REPORT
ACTUAL MEASURED VALUES REFERENCE VALUES

pH 7.354 mm/Hg 7.35 – 7.45 mm/Hg

pCO2 27 mmHg 35 – 45 mm/Hg
pO2 89.1 mmHg 80 – 105 mm/Hg
TCO2 15.5 mmol/L 23 – 27 mmol/L
cHCO3 14.7 mmol/L 22 – 26 mmol/L
cBE - 8.9 mmol/L
SO2 97.0 % 95 – 98 %
 October 12, 2018
RADIOLOGY REPORT
CHEST PA

Clear lung fields.

Normal hilar vessels and mediastinum
Heart is not enlarged.
Thoracic cage, diaphragm and costophrenic sulci are remarkable
IMPRESSION: * No significant chest findings.
 October 12, 2018
URINALYSIS
Color Yellow
Transparency SL.turbid
Sp. Gravity 1.030
pH 6.0
Protein Negative
Sugar Negative
Pus Cells 0 – 3 /hpf
RBC Cells 0 – 2 /hpf
Epithelial Cells Rare
Bacteria Few
A. Urates Few
M. Threads Few
Others Calcium exalate
Few / lpf
 October 12, 2018
BLOOD CHEMISTRY
Sodium 141.1 135 – 145 mmol/L
Potassium 4.07 3.5 – 5.5 mmol/L
Ionized 1.19 1.12- 1.20 mmol/L
Calcium
BUN 5.2 3.2-7.1 mmol/L
Creatinine 66 58-110 mmol/L
 BLOOD CHEMISTRY
TSH LESS THAN 0.05 0.25-5.0 uUI/mL
FT3 17.79 4.0-8.3 pmol/L

FT4 49.66 9.0-20.0 pmol/L

1st hospital day( OCT 13,2018)
S: #1:BODY WEAKNESS
-No lower & upper extremities weakness
-No vomiting, No diarrhea
-No dyspnea
-No fever

O: Conscious, coherent, not in distress, afebrile with the following VS:

BP=120/70mmhg,HR=86bpm,RR=21,temp=36.5C
skin: good turgor, no active lesion
HEENT: pinkish palpebral conjunctiva ,anicteric sclera
Chest & lungs: symmetric lung expansion, clear breath sounds
Cardiac: adynamic precordium, no murmur
Abdomen: flabby ,soft, normoactive bowel sounds
Extremity: full & equal pulses,no edema

MMT: 5/5 both upper & lower extremities

A: Hypokalemic periodic paralysis-RESOLVED-
P: - Refer to an Endocrinologist
D/C potassium drip & oral potassium replacement
- Was given methimazol 20mg 1 tab once a day
Additional work up:
- For ultrasound of the thyroid
Laboratories

ULTRASOUND

Whole abdominal ultrasoud INTRINSICALLY NORMAL ABDOMINAL UTRASOUND

Thyroid ultrasound CONSIDER HASHIMOTOS THYROIDITIS

2nd hospital day ( OCT 14,2018
S: No body weakness
No diarrhea, no vomiting
No fever
No fine tremors, no palpitations, no dyspnea

O: Seen awake, conscious, not in distress with the following VS:

BP=110/70mmhg,HR=62bpm,RR=21cpm,Temp=36.5C
Skin: good turgor, no active lesion
Heent: pinkish palpebral conjunctva, anicteric sclera
Chest: Symmetric lung expansion, clear breath sounds
Cardiac: adynamic precordium, no murmur
Abdomen: flabby, soft, normoactive bowel sounds
Extremity: full & equal pulses, no edema
MMT: 5/5 of both upper & lower extremities
A: Thyrotoxic Hypokalemic Periodic Paralysis-stable
P: Continue methimazole 20 mg 1 tablet OD
MAY GO HOME
DISCUSSION
Hypokalemic periodic paralysis
(HypoKPP) –HARRISONS 18TH ED p.3504
 Onset occurs at adolescence.
 Men are more often affected because of decreased penetrance in women.
 Episodic weakness with onset after age 25 is almost never due to periodic paralyses,
with the exception of thyrotoxic periodic paralysis.
 Attacks are often provoked by meals high in carbohydrates or sodium and may
accompany rest following prolonged exercise.
 Weakness usually affects proximal limb muscles more than distal.
 Ocular and bulbar muscles are less likely to be affected.
 Respiratory muscles are usually spared but when they are involved, the condition may
prove fatal.
 Weakness may take as long as 24 hours to resolve.
 Life-threatening cardiac arrhythmias related to hypokalemia may occur during attacks.
 As a late complication, patients commonly develop severe, disabling proximal lower
extremity weakness

 Attacks of thyrotoxic periodic paralysis resemble those of primary HypoKPP. Despite a higher
incidence of thyrotoxicosis in women, men, particularly those of Asian descent, are more
likely to manifest this complication.

 Attacks abate with treatment of the underlying thyroid condition.

 A low serum potassium level during an attack, excluding secondary causes, establishes the
diagnosis.
Treatment

 Muscle strength and ECG should be monitored

 Oral KCl (0.2–0.4 mmol/kg) should be given every 30 minutes
 Only rarely is IV therapy necessary (e.g., when swallowing problems or
vomiting is present).
 lowcarbohydrate, low-sodium diet and consequences of intense exercise.
 Prophylactic administration of acetazolamide (125–1000 mg/d in divided
doses)
 Review on :Hyperthyroidism

Thyrotoxicosis is a hypermetabolic state caused by elevated circulating levels of free T3

and T4; it is most commonly due to primary hyperactivity of the thyroid (hyperthyroidism)
1.Thyroid hyperplasia (Graves disease; 85% of cases) •
2. Hyperfunctional multinodular goiter
3.Hyperfunctional thyroid adenoma
 Disorders associated with thyrotoxicosis

Primary Secondary Not associated

1. Diffuse hyperplasia(graves TSH secreting pituitary 1.Granulomatousb(de

disease) adenoma quervain) thyroiditis
2. Hyperfunctioning 2. Subacute lymphocytic
multinodular goiter thyroiditis
3. Hyperfunctioning 3. Struma ovarii (ovarian
adenoma teratoma with ectopic
4. Iodine induced thyroid)
hyperthyroidism 4. Factitious thyrotoxicosis
5. Neonatal thyrotoxicosis
associatedc with maternal
graves disease
Clinical course

 Cardiac: Increased cardiac contractility and increased peripheral oxygen

requirements can cause cardiomegaly, tachycardia, palpitations, and arrhythmias
(particularly atrial fibrillation); congestive failure may supervene, particularly
with pre-existing cardiac disease.
 Ocular: Wide, staring gaze and lid lag are due to sympathetic overstimulation of
the levator palpebrae superioris; patients with Graves disease can also have a
deposition ophthalmopathy
 Neuromuscular: Sympathetic nervous system overactivity (with increased b-
adrenergic tone) causes tremor, hyperactivity, emotional lability, anxiety, inability
to concentrate, and insomnia. Proximal muscle weakness and diminished mass are
also common.
 Cutaneous: Increased blood flow and peripheral vasodilation leads to warm, moist,
and flushed skin; Graves patients can also develop an infiltrative dermopathy.
Clinical course

 Gastrointestinal: Hypermotility, malabsorption, and diarrhea are due to

sympathetic hyperstimulation
 Sketelal: Enhanced bone resorption leads to osteoporosis and increased risk of
fractures.
 Thyroid storm: This designates abrupt onset of severe hyperthyroidism; it
usually occurs in Graves patients due to acute elevation in circulating
catecholamines (e.g., secondary to injury, surgery, infection, or any
exogenous stress) and is a medical emergency due to the risk of fatal
arrhythmia.
 Apathetic hyperthyroidism: refers to thyrotoxicosis occuring in older adults in
whim advanced age and various comorbidities may blunt the features of
thyroid hormone excess that typically bring younger patients to attention
Diagnosis

 TSH concentration is the most usefule single screening test for

hyperthyroidism, because its levels are decreased even at the earliest stages.
 Low TSH value is usually confirmed with measurement of free T4 which is
predicably increased.
Graves disease

 This is the most common cause of endogenous hyperthyroidism; a clinical

triad includes:
 Hyperthyroidismduehyperfunctional, diffuse thyroid enlargement
 Infiltrative ophthalmopathy with resultant exophthalmos
 Localized infiltrative dermopathy present in a minority of patients
 Women are affected seven times more frequently than men
 peak incidence is between ages 20 and 40 years with the disease affecting up
to 2% of American women
Pathogenesis

 Graves disease is an autoimmune disorder caused predominantly by

autoantibodies directed against the TSH receptor (TSHR):
 • Thyroid-stimulating immunoglobulin binds to the TSHR and mimics the
action of TSH, leading to T3 and T4 release. It is relatively specific for Graves
disease
 • Thyroid growth-stimulating immunoglobulin is also directed against TSHR,
but these autoantibodies induce thyroid follicular epithelium proliferation.
 • TSH-binding inhibitor immunoglobulin binds to TSHR and prevents TSH from
interacting with the receptor. Such antibodies can mimic TSH (stimulating
thyroid epithelial activity) or can inhibit thyroid cell function.
Treatment
Anti thyroid drugs

 The main antithyroid drugs are the thionamides, such as:

 1.)Propylthiouracil,
 2.)Carbimazole and
 3.)Methimazole.

 All inhibit the function of TPO, reducing oxidation and organification of

iodide.

 also reduce thyroid antibody levels and enhance rates of remission.

 Propylthiouracil inhibits deiodination of T4 → T3.

 There are many variations of antithyroid drug regimens.
 carbimazole or methimazole is usually 10–20 mg every 8 or 12 h
 Propylthiouracil is given at a dose of 100–200 mg every 6–8 hours,
 The starting dose of antithyroid drugs can be gradually reduced as
thyrotoxicosis improves.

 high doses may be given combined with levothyroxine supplementation to

avoid drug-induced hypothyroidism.
 Thyroid function tests are reviewed 4–6 weeks after starting treatment,

 Most patients do not achieve euthyroidism until 6–8 weeks after

 The usual daily maintenance doses of antithyroid drugs in the titration

regimen are :

1.)2.5–10 mg of carbimazole or methimazole and
 2.)50–100 mg of propylthiouracil.
 Maximum remission rates are achieved by 12–18 months and 6 months for the
block-replace regimen.

 Younger patients, males, smokers, and

 with severe hyperthyroidism and

 large goiters

 are most likely to relapse when treatment stops,

2.)Radioiodine

 causes progressive destruction of thyroid cells

 used as initial treatment or
 for relapses after a trial of antithyroid drugs

 risk of thyrotoxic crisis after radioiodine, can be minimized by

pretreatment with antithyroid drugs for at least a month before
treatment.

 Carbimazole or methimazole must be stopped 3–5 days before radioiodine

administration

 Propylthiouracil should be stopped for a longer period before radioiodine

is given
3.)Subtotal or near-total
thyroidectomy
 for patients who relapse after antithyroid drugs and prefer this treatment
to radioiodine.

 particularly when the goiter is very large.

 The major complications of surgery—bleeding, laryngeal edema,

hypoparathyroidism, and damage to the recurrent laryngeal nerves
Thyrotoxic hypokalemic periodic
paralysis:
Thyrotoxic Hyperkalemic Periodic Paralysis (TPP) is an uncommon disorder with
three characteristics which occur at the same time:
 too much thyroid hormone
 low levels of potassium in the blood (hypokalemia)
 muscle weakness or paralysis
Epidemiology

 occurs most often in:

 males of Asian descent, including Japanese, Chinese, Vietnamese, Korean
and Filipinos.
 It also occurs more frequently in those of Native American and Latin American
descent, but only occasionally in those of European descent
Genetics:

The condition has been linked with

 genetic mutations in genes that code for certain ion
channels that transport electrolytes across cell
membranes.
 The main ones are the L-type calcium channel α1-subunit
and potassium inward rectifier 2.6; classified as a
channelopathy
 The abnormality in the channel is thought to lead to shifts
of potassium into cells, under conditions of high thyroxine
levels, usually with an additional precipitant.
 Clinical manifestation
General:

Male predominance; initiation at age 20 to 40

Periodic flaccid paralysis of proximal muscles, mainly of lower extremities

Negative family history of similar symptoms

Hypertension

Subtle clinical features of hyperthyroidism

Laboratory findings:

Hypokalemia, hypophosphatemia, and mild hypomagnesemia

Normal acid-base balance

Low potassium excretion rate (low urinary potassium—creatinine ratio and low TTKG)

Hypercalciuria and hypophosphaturia

Abnormal thyroid function tests (low TSH; elevated free and total T4 and T3; increased T3 uptake)

Electrocardiographic abnormalities:

Sinus tachycardia

Hypokalemic changes: prominent U wave, prolonged PR interval, increased P-wave amplitude, widened QRS complexes

First-degree atrioventricular block

Atrial and ventricular arrhythmias

Pathophysiology
Treatment and management
1. The administration of oral and/or intravenous (IV) potassium is recommended during the
paralysis crisis to accelerate the recovery and prevent a possible cardiac arrhythmia.
2. The oral use of potassium should be preferred, but if a faster recovery is necessary,
potassium may be slowly IV infused, usually over 2 hours. The main concern about
potassium replacement is rebound hyperkalemia because the potassium abnormality is not
due to total potassium depletion but intracellular ion trapping. Therefore, monitoring the serum
K levels during the treatment and suspending the infusion at the first sign of the muscular
force recovery is recommended.
3. Non-selective beta blockers, especially oral propranolol (80-240 mg/day), may be useful in
TPP treatment, especially when awaiting the FT4 and TSH results, by limiting the time of
the crisis without inducing rebound hyperkalemia. These drugs block the adrenergic
stimulation of the Na+/K+-ATPase pump activity, resulting in lower K influx to skeletal
muscle.
4. Early treatment for the underlying cause of thyrotoxicosis is the most important procedure
in patients with TPP. When euthyroidism is reached, the paralysis crises remits definitively.
5. Triggering factors such as high intake of carbohydrates, alcohol, and intense physical
exercise should be avoided until the resolution of the thyroid disease.
6. In cases of thyrotoxicosis caused by excessive intake of thyroid hormones, the drug is
suspended. In hyperthyroidism
References

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hypokalemic periodic paralysis, an endocrine emergency: clinical and genetic
features in 25 patients. Arquivos brasileiros de endocrinologia e metabologia
2004;48:196-215.
 [2] Maciel RM, Lindsey SC, Dias da Silva MR. Novel etiopathophysiological aspects of
thyrotoxic periodic paralysis. Nat Rev Endocrinol 2011;7:657-67.
 [3] Hay ID, McDougall IR. Letter: Thyrotoxic periodic paralysis in Britain. British
medical journal 1975;4:761.
 [4] Hackshaw KV, Coker E. Hypokalemic periodic paralysis in a hyperthyroid black
woman. Journal of the National Medical Association 1988;80:1343-4.
 [5] Lin SH. Thyrotoxic periodic paralysis. Mayo Clin Proc 2005;80:99-105.
 [6] Rosenfeld M. Akute aufsteigende Lahmungen bei Morbus Basedow. Berl Klin
Wochenschr 1902;39:538-40.
 [7] Dunlap HF, Kepler EJ. A syndrome resembling familial periodic paralysis occurring
in the course of exolphthalmic goiter. Endocrinology 1931;15:541-6.