Blood Film Abnormalities and Their Significance

Blood film abnormalities can provide important diagnostic information about a patient’s health. One such abnormality is Howell-Jolly bodies, which are nuclear remnants found in red blood cells and indicate hyposplenism. Other abnormalities seen in hyposplenism include target cells, Pappenheimer cells, increased red cell anisocytosis and poikilocytosis, and spherocytes. Patients with hyposplenism are at increased risk of bacterial infections and should be vaccinated accordingly.

Rouleaux formation, on the other hand, is a stack of red blood cells that stick together, forming a rouleau. This occurs in conditions where plasma protein is high, such as multiple myeloma, some infections, Waldenström’s macroglobulinemia, and some cancers.

Schistocytes are irregular and jagged fragments of red blood cells that occur due to mechanical destruction of red blood cells in conditions such as hemolytic anemia. They are not typically seen in hyposplenism.

Tear drop cells, which are seen in conditions where there is abnormality of bone marrow function, such as myelofibrosis, are also not seen in hyposplenism.

Finally, toxic granulation occurs during inflammatory processes such as bacterial infection or sepsis and refers to neutrophils which contain dark, coarse granules. It is not present in hyposplenism.

In summary, understanding blood film abnormalities and their significance can aid in the diagnosis and management of various medical conditions.

Differential Diagnosis for Pulmonary Granulomas and Positive c-ANCA: A Case Study

Granulomatosis with polyangiitis (GPA) is a rare autoimmune disease that often presents with granulomatous lung disease and alveolar capillaritis. Symptoms include cough, dyspnea, hemoptysis, and chest pain. Chest X-ray and computed tomography can show rounded lesions that may cavitate, while bronchoscopy can reveal granulomatous inflammation. In this case study, the chest radiograph appearances, epistaxis, and positive c-ANCA are more indicative of GPA than lung cancer, echinococcosis, systemic lupus erythematosus, or tuberculosis. While SLE can also cause pulmonary manifestations, cavitating lesions are not typical. Positive c-ANCA is associated with GPA, while SLE is associated with positive antinuclear antibodies, double-stranded DNA antibodies, and extractable nuclear antigens.

A child under the age of 3 who presents with an acute limp requires urgent specialist assessment. This is because septic arthritis is more common than transient synovitis in this age group. A routine paediatric referral is not appropriate as the concern is ruling out septic arthritis, which requires urgent attention. An urgent X-ray or hip ultrasound scan is also not sufficient, as a comprehensive specialist examination is necessary to exclude serious pathology.

Causes of Limping in Children

Limping in children can be caused by various factors, which may differ depending on the child’s age. One possible cause is transient synovitis, which has an acute onset and is often accompanied by viral infections. This condition is more common in boys aged 2-12 years. On the other hand, septic arthritis/osteomyelitis may cause a child to feel unwell and have a high fever. Juvenile idiopathic arthritis may cause a painless limp, while trauma can usually be diagnosed through the child’s history. Development dysplasia of the hip is usually detected in neonates and is six times more common in girls. Perthes disease, which is due to avascular necrosis of the femoral head, is more common in children aged 4-8 years. Finally, slipped upper femoral epiphysis may occur in children aged 10-15 years and is characterized by the displacement of the femoral head epiphysis postero-inferiorly. It is important to identify the cause of a child’s limp in order to provide appropriate treatment and prevent further complications.

Treatment Options for Ulcerative Colitis

Ulcerative colitis (UC) is a chronic inflammatory bowel disease that affects the rectum and may spread to the colon. The main symptom is bloody diarrhea, and the disease follows a relapsing and remitting course. The goal of UC management is to treat acute relapses, prevent relapses, and detect cancers early.

Mesalazine is an effective first-line treatment for mild to moderate UC, which involves enemas and oral medication. For moderately active cases, oral aminosalicylates, topical aminosalicylates, and corticosteroids are used. Azathioprine is an immunomodulator that is rarely used to induce remission but is used to keep patients in remission. Hydrocortisone is a systemic steroid used for severe cases. Infliximab is an anti-tumor necrosis factor biologic used for moderate to severe cases that are refractory to standard treatment. Methotrexate is an alternative immunomodulator for patients who cannot tolerate azathioprine. It is important to discuss adequate contraception with patients on methotrexate due to its teratogenicity.

Understanding Treatment Options for Ulcerative Colitis

Atropine is the primary antidote for organophosphate insecticide poisoning. It works by competitively inhibiting cholinergic activation and requires gradual dose escalation until respiratory symptoms improve. In cases where high-dose atropine is ineffective, adrenaline may be used, although there is limited evidence to support this approach. Diazepam may be used prophylactically to minimize neurocognitive dysfunction, but it would not be effective in this case as the patient is not experiencing seizures and requires treatment with atropine to address respiratory distress. Methylene blue is reserved for severe cases of methemoglobinemia, which is not indicated by the patient’s history or physical examination.

Understanding Organophosphate Insecticide Poisoning

Organophosphate insecticide poisoning is a condition that occurs when there is an accumulation of acetylcholine in the body, leading to the inhibition of acetylcholinesterase. This, in turn, causes an upregulation of nicotinic and muscarinic cholinergic neurotransmission. In warfare, sarin gas is a highly toxic synthetic organophosphorus compound that has similar effects. The symptoms of organophosphate poisoning can be remembered using the mnemonic SLUD, which stands for salivation, lacrimation, urination, and defecation/diarrhea. Other symptoms include hypotension, bradycardia, small pupils, and muscle fasciculation.

The management of organophosphate poisoning involves the use of atropine, which helps to counteract the effects of acetylcholine. However, the role of pralidoxime in the treatment of this condition is still unclear. Meta-analyses conducted to date have failed to show any clear benefit of pralidoxime in the management of organophosphate poisoning.

Management of Head Injury: Importance of CT Scan and Neuro Observation

Head injury is a serious medical condition that requires prompt and appropriate management. The current imaging modality used to investigate brain injury is CT. According to the National Institute for Health and Care Excellence (NICE) head injury guidelines, patients who sustained a head injury and have any of the following risk factors should be scanned within 1 hour: GCS <13 on initial assessment in the Emergency Department, GCS <15 at 2 hours after the injury on assessment in the Emergency Department, suspected open or depressed skull fracture, any sign of basal skull fracture, post-traumatic seizure, focal neurological deficit, and more than one episode of vomiting. A provisional radiology report should be given to the requesting clinician within 1 hour of the scan performed to aid immediate clinical management. While waiting for the CT scan, the patient should be monitored using a neuro observation chart, and any deterioration needs to be immediately reported to the responsible clinician for the patient’s care. Admitting the patient for neuro observation is crucial to ensure prompt management of any changes in the patient’s condition. There is no indication to discuss the patient with the neurosurgical department at present. Once the imaging has been performed and if new surgically significant intracranial pathology is detected, then discussion of the care plan should take place with the local neurosurgical team. Discussion of the care plan with a neurosurgeon is warranted, regardless of imaging, if any of the following is present: GCS 8 or less persisting despite initial resuscitation, unexplained confusion lasting >4 hours, deterioration in GCS score after admission, progressing focal neurological signs, a seizure without full recovery, CSF leak, suspected/definitive.

In conclusion, the immediate CT scan and neuro observation are crucial steps in the management of head injury. Discharging a patient with a high-risk head injury is inappropriate and can lead to serious consequences.

As a medical student, you may not be required to interpret fetal CTGs, but you should have a basic understanding of their purpose and key features. A CTG measures fetal heart rate and uterine contractions and is used when there are risk factors for fetal hypoxia. While CTGs are not specific and can lead to increased medical intervention, changes in fetal heart rate should be taken seriously as they indicate fetal distress.

To interpret a CTG, you can use the mnemonic DR C BRA VADO. DR stands for defining the patient’s risk factors for being on a CTG monitor, while C refers to counting the number of contractions in 10 minutes. BRA stands for baseline rate and variability, with a normal fetal baseline rate being 110-160 beats per minute and variability ranging from 5 to 25 beats per minute. A refers to accelerations, which are rises in fetal heart rate, and D refers to decelerations, which are reductions in fetal heart rate. Late decelerations, which are slow to recover, are particularly concerning as they indicate fetal hypoxia.

As a medical student, it is important to be aware of terminal bradycardia and terminal decelerations, which are indicators for emergency caesarean section. Other changes in CTG features are usually investigated with fetal scalp blood sampling and an ABG to check for acidosis. The NICE guidelines provide a useful table for interpreting CTG features and determining appropriate management, ranging from normal care to urgent intervention.

Cardiotocography (CTG) is a medical procedure that measures pressure changes in the uterus using either internal or external pressure transducers. It is used to monitor the fetal heart rate, which normally ranges between 100-160 beats per minute. There are several features that can be observed during a CTG, including baseline bradycardia (heart rate below 100 beats per minute), which can be caused by increased fetal vagal tone or maternal beta-blocker use. Baseline tachycardia (heart rate above 160 beats per minute) can be caused by maternal pyrexia, chorioamnionitis, hypoxia, or prematurity. Loss of baseline variability (less than 5 beats per minute) can be caused by prematurity or hypoxia. Early deceleration, which is a decrease in heart rate that starts with the onset of a contraction and returns to normal after the contraction, is usually harmless and indicates head compression. Late deceleration, on the other hand, is a decrease in heart rate that lags behind the onset of a contraction and does not return to normal until after 30 seconds following the end of the contraction. This can indicate fetal distress, such as asphyxia or placental insufficiency. Variable decelerations, which are independent of contractions, may indicate cord compression.

A false positive VDRL/RPR result can occur due to various reasons such as SLE, TB, malaria, and HIV. In this case, the patient’s positive VDRL result is likely due to SLE, which can cause non-specific antibodies and lead to a false-positive result. However, azathioprine use or progesterone-only pill use would not affect the VDRL test and are not responsible for the false-positive syphilis result. It is important to note that STI testing can be done 4 weeks after sexual intercourse, and in this case, the results can be interpreted as the patient had her last unprotected sexual encounter 5 weeks ago.

Syphilis Diagnosis: Serological Tests

Syphilis is caused by Treponema pallidum, a bacterium that cannot be grown on artificial media. Therefore, diagnosis is based on clinical features, serology, and microscopic examination of infected tissue. Serological tests for syphilis can be divided into non-treponemal tests and treponemal-specific tests. Non-treponemal tests are not specific for syphilis and may result in false positives. They assess the quantity of antibodies being produced and become negative after treatment. Examples of non-treponemal tests include rapid plasma reagin (RPR) and Venereal Disease Research Laboratory (VDRL). On the other hand, treponemal-specific tests are more complex and expensive but are specific for syphilis. They are qualitative only and are reported as either reactive or non-reactive. Examples of treponemal-specific tests include TP-EIA and TPHA.

The testing algorithms for syphilis are complicated but typically involve a combination of a non-treponemal test with a treponemal-specific test. False positive non-treponemal tests may occur due to pregnancy, SLE, antiphospholipid syndrome, tuberculosis, leprosy, malaria, or HIV. A positive non-treponemal test with a positive treponemal test is consistent with an active syphilis infection. A positive non-treponemal test with a negative treponemal test is consistent with a false-positive syphilis result, such as due to pregnancy or SLE. A negative non-treponemal test with a positive treponemal test is consistent with successfully treated syphilis.

If a patient presents with a paracetamol overdose more than 24 hours after the incident and shows signs of jaundice or hepatic tenderness, immediate administration of N-acetylcysteine (NAC) is necessary. Waiting for blood test results is not recommended in such cases. However, if the patient does not show any signs of liver toxicity, treatment can be initiated based on the results of blood tests, specifically if the ALT level is above the normal limit. Waiting for the detection of serum paracetamol concentration is also not recommended. While psychiatric assessment is important for all patients with non-accidental overdose, in this case, the priority should be the immediate treatment of liver toxicity with NAC.

Paracetamol overdose management guidelines were reviewed by the Commission on Human Medicines in 2012. The new guidelines removed the ‘high-risk’ treatment line on the normogram, meaning that all patients are treated the same regardless of their risk factors for hepatotoxicity. However, for situations outside of the normal parameters, it is recommended to consult the National Poisons Information Service/TOXBASE. Patients who present within an hour of overdose may benefit from activated charcoal to reduce drug absorption. Acetylcysteine should be given if the plasma paracetamol concentration is on or above a single treatment line joining points of 100 mg/L at 4 hours and 15 mg/L at 15 hours, regardless of risk factors of hepatotoxicity. Acetylcysteine is now infused over 1 hour to reduce adverse effects. Anaphylactoid reactions to IV acetylcysteine are generally treated by stopping the infusion, then restarting at a slower rate. The King’s College Hospital criteria for liver transplantation in paracetamol liver failure include arterial pH < 7.3, prothrombin time > 100 seconds, creatinine > 300 µmol/l, and grade III or IV encephalopathy.

Possible Diagnoses for a Pyrexial Patient with Chest Signs

A pyrexial patient with chest signs on the right-hand side may have ventilator-acquired pneumonia, which occurs due to contamination of the respiratory tract from oropharyngeal secretions. Diagnosis is based on clinical examination, X-ray, blood culture, and bronchial washings. Initial antibiotic therapy should cover anaerobes, MRSA, Pseudomonas, and Acinetobacter.

If the patient has been in the hospital for more than 72 hours, any infection that develops is likely to be hospital-acquired.

Acute respiratory distress syndrome (ARDS) presents more acutely and broncholavage samples commonly demonstrate inflammatory and necrotic cells.

Infective pulmonary edema is unlikely if there are no indications of pleural effusions or edema on clinical examination and chest radiograph.

Pulmonary hemorrhage is unlikely if there is no blood found in the bronchial aspirates.

Possible Diagnoses for a Pyrexial Patient with Chest Signs

Acetylcholinesterase Inhibitors and Muscarinic Effects

An acetylcholinesterase inhibitor, also known as an anticholinesterase, is a chemical that prevents the breakdown of acetylcholine (ACh) by inhibiting the cholinesterase enzyme. This leads to an increase in both the level and duration of action of ACh, a neurotransmitter that stimulates postganglionic receptors to produce various effects such as salivation, lacrimation, defecation, micturition, sweating, miosis, bradycardia, and bronchospasm. These effects are referred to as muscarinic effects, and the postganglionic receptors are called muscarinic receptors since muscarine produces these effects.

One pathological syndrome associated with excessive stimulation of the parasympathetic nervous system is SLUD, which stands for Salivation, Lacrimation, Urination, Defecation, and emesis. SLUD is not likely to occur naturally and is usually encountered only in cases of drug overdose or exposure to nerve gases. Nerve gases irreversibly inhibit the acetylcholinesterase enzyme, leading to a chronically high level of ACh at cholinergic synapses throughout the body. This, in turn, chronically stimulates ACh receptors throughout the body, resulting in SLUD and other muscarinic effects.

Diagnostic Tests for Coeliac Disease

Coeliac disease is a condition that affects the small intestine and is caused by an intolerance to gluten. There are several diagnostic tests available to help establish a diagnosis of coeliac disease. The first line test is the IgA tissue transglutaminase (tTGA) antibody serology. A positive test indicates that further testing, such as endoscopy and biopsy, is needed for confirmation.

Before testing, it is important to confirm that the patient has been consuming gluten-containing foods regularly for at least six weeks. HLA testing is not a first line test and should only be carried out in secondary care.

If the tTGA test is unavailable or weakly positive, IgA endomysial antibody testing may be used as a second line test. Small bowel biopsy is only indicated if serology is positive or equivocal.

There is no indication for an abdominal CT scan in this scenario. The first line investigation for coeliac disease is serology, and if positive, diagnosis is confirmed or excluded by biopsy of the small bowel at endoscopy.

Ultrasound is the key investigation for pyloric stenosis, as other methods such as abdominal x-ray, CT scans, TTG antibodies, and upper GI contrast study are less useful or not applicable for young children with this condition. The classic symptom of pyloric stenosis is forceful projectile vomiting.

Understanding Pyloric Stenosis

Pyloric stenosis is a condition that usually occurs in infants between the second and fourth weeks of life. However, in rare cases, it may present later, up to four months. This condition is caused by the thickening of the circular muscles of the pylorus. Pyloric stenosis is more common in males, with an incidence of 4 per 1,000 live births. It is also more likely to affect first-borns and infants with a positive family history.

The most common symptom of pyloric stenosis is projectile vomiting, which usually occurs about 30 minutes after a feed. Other symptoms may include constipation, dehydration, and a palpable mass in the upper abdomen. Prolonged vomiting can lead to hypochloraemic, hypokalaemic alkalosis, which can be life-threatening.

Diagnosis of pyloric stenosis is typically made using ultrasound. Management of this condition involves a surgical procedure called Ramstedt pyloromyotomy. This procedure involves making a small incision in the pylorus to relieve the obstruction and allow for normal passage of food. With prompt diagnosis and treatment, infants with pyloric stenosis can make a full recovery.

White kite, bright light, tight fight – these are examples of clang associations, where words are linked by their similar sounds or rhymes. It is a symptom often seen in individuals with schizophrenia or bipolar disorder. However, this patient is not currently displaying any signs of psychosis or mania. It is important to note that aphasic speech, where the patient loses the ability to form language, and echolalia, where they repeat words or phrases of others, are different from clang associations.

Thought disorders can manifest in various ways, including circumstantiality, tangentiality, neologisms, clang associations, word salad, Knight’s move thinking, flight of ideas, perseveration, and echolalia. Circumstantiality involves providing excessive and unnecessary detail when answering a question, but eventually returning to the original point. Tangentiality, on the other hand, refers to wandering from a topic without returning to it. Neologisms are newly formed words, often created by combining two existing words. Clang associations occur when ideas are related only by their similar sounds or rhymes. Word salad is a type of speech that is completely incoherent, with real words strung together into nonsensical sentences. Knight’s move thinking is a severe form of loosening of associations, characterized by unexpected and illogical leaps from one idea to another. Flight of ideas is a thought disorder that involves jumping from one topic to another, but with discernible links between them. Perseveration is the repetition of ideas or words despite attempts to change the topic. Finally, echolalia is the repetition of someone else’s speech, including the question that was asked.

Carbamazepine induces the P450 enzyme. This enzyme system includes CYP3A4, which metabolizes ethinylestradiol, a component of the combined oral contraceptive (COC) pill. Induction of P450 enzymes accelerates the breakdown of ethinylestradiol, reducing the effectiveness of the COC pill. On the other hand, ciprofloxacin and omeprazole inhibit P450 enzymes, slowing down the breakdown of P450 enzyme substrates. Propranolol is a P450 enzyme substrate, but it does not affect the efficacy of the enzyme system.

P450 Enzyme System and its Inducers and Inhibitors

The P450 enzyme system is responsible for metabolizing drugs in the body. Induction of this system usually requires prolonged exposure to the inducing drug, unlike P450 inhibitors, which have rapid effects. Some drugs that induce the P450 system include antiepileptics like phenytoin and carbamazepine, barbiturates such as phenobarbitone, rifampicin, St John’s Wort, chronic alcohol intake, griseofulvin, and smoking, which affects CYP1A2 and is the reason why smokers require more aminophylline.

On the other hand, some drugs inhibit the P450 system, including antibiotics like ciprofloxacin and erythromycin, isoniazid, cimetidine, omeprazole, amiodarone, allopurinol, imidazoles such as ketoconazole and fluconazole, SSRIs like fluoxetine and sertraline, ritonavir, sodium valproate, and acute alcohol intake. It is important to be aware of these inducers and inhibitors as they can affect the metabolism and efficacy of drugs in the body. Proper dosing and monitoring can help ensure safe and effective treatment.

Maternal and Paternal Inheritance in Chromosomal Abnormalities

In certain chromosomal abnormalities, the source of the extra chromosome can be traced back to either the mother or the father. In Klinefelter’s syndrome, where there is an extra X chromosome, the maternal source accounts for about 60% of cases. This is a higher percentage compared to other possibilities. Trisomy 21, which is also known as Down syndrome, is maternally derived in 95% of cases. On the other hand, trisomy 13 and 18 are more commonly derived from the mother. In the case of 47,XYY, where there is an extra Y chromosome, the extra chromosome comes from the father. the source of the extra chromosome can provide insight into the genetic mechanisms behind these chromosomal abnormalities. By identifying the source, it may also be possible to predict the likelihood of recurrence in future pregnancies.

The appropriate management for acute limb ischaemia involves administering analgesia, IV heparin, and requesting a vascular review. Paracetamol and codeine should not be given as the patient’s condition requires urgent attention to prevent fatal consequences for the limb. IV heparin is necessary to prevent thrombus propagation, and the patient must be seen by the vascular team for potential definitive management, such as intra-arterial thrombolysis or surgical embolectomy. Paracetamol, iloprost, and atorvastatin are not suitable for this condition as they are used to manage Raynaud’s phenomenon. Requesting a vascular review alone is not enough as analgesia is also required to alleviate pain.

Peripheral arterial disease can present in three main ways: intermittent claudication, critical limb ischaemia, and acute limb-threatening ischaemia. The latter is characterized by one or more of the 6 P’s: pale, pulseless, painful, paralysed, paraesthetic, and perishing with cold. Initial investigations include a handheld arterial Doppler examination and an ankle-brachial pressure index (ABI) if Doppler signals are present. It is important to determine whether the ischaemia is due to a thrombus or embolus, as this will guide management. Thrombus is suggested by pre-existing claudication with sudden deterioration, reduced or absent pulses in the contralateral limb, and evidence of widespread vascular disease. Embolus is suggested by a sudden onset of painful leg (<24 hours), no history of claudication, clinically obvious source of embolus, and no evidence of peripheral vascular disease. Initial management includes an ABC approach, analgesia, intravenous unfractionated heparin, and vascular review. Definitive management options include intra-arterial thrombolysis, surgical embolectomy, angioplasty, bypass surgery, or amputation for irreversible ischaemia.

Differential diagnosis of a patient with liver disease and neurological symptoms

Wilson’s disease, haemochromatosis, alcohol-related cirrhosis, viral hepatitis, and primary sclerosing cholangitis are among the possible causes of liver disease. In the case of a patient with Kayser-Fleischer rings, the likelihood of Wilson’s disease increases, as this is a characteristic sign of copper overload due to defective incorporation of copper and caeruloplasmin. Neurological symptoms such as disinhibition, emotional lability, and chorea may also suggest Wilson’s disease, although they are not specific to it. Haemochromatosis, which is characterized by iron overload, can be ruled out if the ferritin level is normal. Alcohol-related cirrhosis is less likely if the patient denies alcohol or drug abuse, but this information may not always be reliable. Viral hepatitis is a common cause of liver disease, but in this case, there are no obvious risk factors in the history. Primary sclerosing cholangitis, which is a chronic inflammatory disease of the bile ducts, does not present with Kayser-Fleischer rings. Therefore, a careful evaluation of the patient’s clinical features, laboratory tests, and imaging studies is necessary to establish the correct diagnosis and guide the appropriate treatment.

Diagnostic Investigations for Subarachnoid Haemorrhage

Subarachnoid haemorrhage (SAH) is a medical emergency that requires urgent investigation and management. The following diagnostic investigations are commonly used to diagnose and manage SAH:

CT Scan without Contrast: This is the first line investigation for every patient suspected of having SAH. A positive scan will show a hyperdense area in the basal cisterns. If SAH is confirmed, further imaging with angiography is required to locate the bleed and treat it appropriately.

Fundal Examination: Although fundal examination may show some abnormal findings, it is not a diagnostic investigation for SAH.

MRI Scan: MRI scan is considered less optimal for detecting SAH due to longer study times and higher cost implications. The sensitivity of MRI in detecting SAH is thought to be equal or less sensitive to that of CT scanning.

CT Angiogram: A CT angiogram is appropriate after acute SAH is confirmed via CT without contrast. The CT angiogram may then be used to confirm the origin of the bleed.

Lumbar Puncture: In a small percentage of patients with SAH, CT head can be normal. A lumbar puncture should be performed in patients with suspected SAH and a normal CT of the head as long as the CT scan showed no contraindications. The lumbar puncture should ideally be delayed for 4-12 hours to diagnose xanthochromia reliably. Microscopy of the CSF is unreliable because many lumbar punctures are traumatic, and therefore red blood cells will be seen even in the absence of SAH.

Diagnostic Investigations for Subarachnoid Haemorrhage

NICE updated guidelines on antenatal care in 2021, recommending the combined test for screening for Down’s syndrome between 11-13+6 weeks. The test includes nuchal translucency measurement, serum B-HCG, and pregnancy-associated plasma protein A (PAPP-A). The quadruple test is offered between 15-20 weeks for women who book later in pregnancy. Results are interpreted as either a ‘lower chance’ or ‘higher chance’ of chromosomal abnormalities. If a woman receives a ‘higher chance’ result, she may be offered a non-invasive prenatal screening test (NIPT) or a diagnostic test. NIPT analyzes cell-free fetal DNA in the mother’s blood and has high sensitivity and specificity for detecting chromosomal abnormalities. Private companies offer NIPT screening from 10 weeks gestation.